Transistors, the building blocks of modern electronics, are typically made of silicon. Because it’s a semiconductor, this material can control the flow of electricity in a circuit. But silicon has fundamental physical limits that restrict how compact and energy-efficient a transistor can be.

MIT researchers have now replaced silicon with a magnetic semiconductor, creating a magnetic transistor that could enable smaller, faster, and more energy-efficient circuits. The material’s magnetism strongly influences its electronic behavior, leading to more efficient control of the flow of electricity. 

The team used a novel magnetic material and an optimization process that reduces the material’s defects, which boosts the transistor’s performance.

The material’s unique magnetic properties also allow for transistors with built-in memory, which would simplify circuit design and unlock new applications for high-performance electronics.

“People have known about magnets for thousands of years, but there are very limited ways to incorporate magnetism into electronics. We have shown a new way to efficiently utilize magnetism that opens up a lot of possibilities for future applications and research,” says Chung-Tao Chou, an MIT graduate student in the departments of Electrical Engineering and Computer Science (EECS) and Physics, and co-lead author of a paper on this advance.

Chou is joined on the paper by co-lead author Eugene Park, a graduate student in the Department of Materials Science and Engineering (DMSE); Julian Klein, a DMSE research scientist; Josep Ingla-Aynes, a postdoc in the MIT Plasma Science and Fusion Center; Jagadeesh S. Moodera, a senior research scientist in the Department of Physics; and senior authors Frances Ross, TDK Professor in DMSE; and Luqiao Liu, an associate professor in EECS, and a member of the Research Laboratory of Electronics; as well as others at the University of Chemistry and Technology in Prague. The paper appears today in Physical Review Letters.

Overcoming the limits

In an electronic device, silicon semiconductor transistors act like tiny light switches that turn a circuit on and off, or amplify weak signals in a communication system. They do this using a small input voltage.

But a fundamental physical limit of silicon semiconductors prevents a transistor from operating below a certain voltage, which hinders its energy efficiency.

To make more efficient electronics, researchers have spent decades working toward magnetic transistors that utilize electron spin to control the flow of electricity. Electron spin is a fundamental property that enables electrons to behave like tiny magnets.

So far, scientists have mostly been limited to using certain magnetic materials. These lack the favorable electronic properties of semiconductors, constraining device performance.

“In this work, we combine magnetism and semiconductor physics to realize useful spintronic devices,” Liu says.

The researchers replace the silicon in the surface layer of a transistor with chromium sulfur bromide, a two-dimensional material that acts as a magnetic semiconductor.

Due to the material’s structure, researchers can switch between two magnetic states very cleanly. This makes it ideal for use in a transistor that smoothly switches between “on” and “off.”

“One of the biggest challenges we faced was finding the right material. We tried many other materials that didn’t work,” Chou says.

They discovered that changing these magnetic states modifies the material’s electronic properties, enabling low-energy operation. And unlike many other 2D materials, chromium sulfur bromide remains stable in air.

To make a transistor, the researchers pattern electrodes onto a silicon substrate, then carefully align and transfer the 2D material on top. They use tape to pick up a tiny piece of material, only a few tens of nanometers thick, and place it onto the substrate.

“A lot of researchers will use solvents or glue to do the transfer, but transistors require a very clean surface. We eliminate all those risks by simplifying this step,” Chou says.

Leveraging magnetism

This lack of contamination enables their device to outperform existing magnetic transistors. Most others can only create a weak magnetic effect, changing the flow of current by a few percent or less. Their new transistor can switch or amplify the electric current by a factor of 10.

They use an external magnetic field to change the magnetic state of the material, switching the transistor using significantly less energy than would usually be required.

The material also allows them to control the magnetic states with electric current. This is important because engineers cannot apply magnetic fields to individual transistors in an electronic device. They need to control each one electrically.

The material’s magnetic properties could also enable transistors with built-in memory, simplifying the design of logic or memory circuits.

A typical memory device has a magnetic cell to store information and a transistor to read it out. Their method can combine both into one magnetic transistor.

“Now, not only are transistors turning on and off, they are also remembering information. And because we can switch the transistor with greater magnitude, the signal is much stronger so we can read out the information faster, and in a much more reliable way,” Liu says.

Building on this demonstration, the researchers plan to further study the use of electrical current to control the device. They are also working to make their method scalable so they can fabricate arrays of transistors.

This research was supported, in part, by the Semiconductor Research Corporation, the U.S. Defense Advanced Research Projects Agency (DARPA), the U.S. National Science Foundation (NSF), the U.S. Department of Energy, the U.S. Army Research Office, and the Czech Ministry of Education, Youth, and Sports. The work was partially carried out at the MIT.nano facilities.

Fascinating video about searching for life undersea. The video basically makes the point that our bright white searchlights are scaring everything away, and that red light is more neutral. That, plus bait to attract sea creatures, is teaching us a lot about what’s going on down there. Lots of footage of giant squid, and speculation about the colossal squid. Worth watching.

As usual, you can also use this squid post to talk about the security stories in the news that I haven’t covered.

Blog moderation policy.

Every year, lung cancer kills more than 100,000 people in the United States. Smoking is the leading risk factor for lung cancer, but other environmental exposures can also contribute to the disease.

In an advance that could help prevent some of those lung cancer deaths, MIT researchers have shown that blocking an enzyme involved in lung inflammation appears to reduce the risk of developing tumors. 

The researchers found that this enzyme, caspase-1, is active in developing tumors in mice. When they treated the mice with a small-molecule drug that inhibits caspase-1, the mice were much less likely to develop lung tumors.

That drug has already gone into clinical trials for other diseases, and the researchers now hope to test it as a preventative drug in people with elevated risk for lung cancer. 

“If you look at global cancer deaths, lung cancer causes most of them, and most of that is driven by tobacco smoking. Additionally, people who are ‘never smokers’ are showing up with lung cancer. You can imagine a future where you get a test and if you’re deemed high-risk, you go on a preventative medicine. This concept is called cancer interception, and it could help millions of people,” says Sangeeta Bhatia, the John and Dorothy Wilson Professor of Health Sciences and Technology and of Electrical Engineering and Computer Science at MIT, and a member of MIT’s Koch Institute for Integrative Cancer Research and the Institute for Medical Engineering and Science (IMES).

Bhatia is the senior author of the new study, which appears today in Science Advances. Cathy Wang PhD ’26 is the lead author of the paper. 

Blocking inflammation

Preventing lung cancer in patients who are at high risk could significantly reduce the death toll of the disease. In 2017, a clinical trial run by Novartis yielded a tantalizing hint that targeting lung inflammation could prevent some lung cancer cases. That trial, known as CANTOS, was designed to examine whether an anti-inflammatory drug — an antibody that blocks the cytokine IL-1 beta — could reduce the risk of strokes and heart attacks. Unexpectedly, the researchers found that this treatment led to lower rates of lung cancer in a subset of people.

Later trials showed that the antibody had little effect in patients who had established lung cancer, but researchers are still exploring the possibility of using it to prevent progression of lung cancer in high-risk patients. A recent study by the Swanton lab at the Francis Crick Institute identified a set of proteins, across several biological pathways and cell types, that could be used to predict which patients would respond to treatment with an IL-1 beta antibody. 

IL-1 beta requires protease cleavage to be converted to its mature, active form. Thus, Bhatia and her team wondered if enzymes called proteases, which cleave other proteins, might be involved in driving the inflammatory pathway that includes IL-1 beta.

For several years, Bhatia’s lab has been developing tools to track and visualize proteases, since the activity of these enzymes can contribute to cancer development. Proteases can help tumor cells escape their original locations by cutting through proteins of the extracellular matrix, and they also play essential roles in guiding inflammatory cell migration, which can influence tumor growth and immune system targeting.

By coming up with ways to detect these enzymes, Bhatia’s lab has created diagnostic nanosensors for cancer and other diseases. The sensors consist of nanoparticles decorated with peptides that can be cleaved by certain proteases, revealing when proteases are active in a particular tissue or disease state.

In addition to their role in cancer, proteases are known to be involved in the regulation of inflammation. In their new study, Bhatia and her colleagues adapted their nanosensors to identify proteases that may participate in IL-1 beta-mediated inflammatory pathways. 

“We know that proteases are very important in inflammation, and we wanted to pinpoint which ones might be the most active during early lung cancer development,” Wang says.

For this study, the researchers used a mouse model developed by Tyler Jacks, the David H. Koch Professor of Biology at MIT and a member of the Koch Institute. This model, known as KPS, is engineered to turn on cancer-causing mutations in the p53 and Kras genes. The mice also express a peptide called SIINFEKL, which helps to activate T cells and stimulate inflammation in the lung.

The researchers designed their experiments to allow them to model increased cancer risk, beginning before tumor formation was detectable. Five weeks after they induced the cancer-causing mutations, the researchers injected some of the mice with an antibody that blocks IL-1 beta, while others were untreated. Three weeks later, the researchers used their nanosensors to detect proteases that were active in the lungs. 

Those experiments showed that in untreated mice, which all developed lung tumors, caspase-1 was very active. However, in the treated mice, which had fewer tumors, caspase-1 activity was significantly reduced. The researchers also found that in untreated mice, the active caspase-1 was found primarily in lung tumors, not in nearby healthy tissue.

Working with Lecia Sequist, a professor of medicine at Havard Medical School and physician at Mass General Brigham, the researchers also analyzed a small number of human lung fluid samples. In these samples, they also found higher levels of caspase-1 activity from patients with lung cancer compared to healthy donors, despite a common smoking history.

A repurposed drug

The observation that caspase-1 activity is interrelated with the IL-1 beta inflammation pathway was not completely surprising, given IL-1 beta itself required protease cleavage to be converted to its mature, active form. The MIT team then investigated whether inhibitors of caspase-1 might also provide the same protective effects as inhibitors of IL-1 beta, or even improve them. 

Before tumors developed, the researchers began treating the at-risk KPS mice with either a caspase-1 inhibitor, an IL-1 beta antibody, or both. In mice that received both drugs, nearly 20 percent never developed tumors at all. In the mice that received either the caspase-1 inhibitor or the IL-1 beta antibody alone, tumors were much smaller and less numerous than in untreated mice.

Unlike antibodies, which need to be given intravenously, caspase-1 inhibitors can be taken orally, which could make them more appealing as a preventative treatment. Another opportunity provided by these drugs is that they have previously been tested in clinical trials for treatment of rheumatoid arthritis and other diseases.

“What’s so attractive about using this caspase-1 inhibitor is that it has actually been tested in humans. It’s already been through safety studies, and we think it could potentially be repurposed for cancer prevention,” Bhatia says.

The researchers hope to test the drug in a clinical trial, potentially using the biomarkers that were identified by the Swanton team to identify subjects who are likely responsive to IL-1 beta antibody treatment. 

The authors of the study also include MIT researchers Qian Zhong, Shih-Ting Wang, Carmen Martin-Alonso, Sofia Neaher, Sahil Patel, Tiziana Parisi, Jesse Kirkpatrick, and Tyler Jacks. 

The study was funded by Johnson & Johnson, Upstage Lung Cancer through the Koch Institute Frontier Research Program, the Virginia and D.K. Ludwig Fund for Cancer Research, the Koch Institute’s Marble Center for Cancer Nanomedicine, the Koch Institute Support (core) Grant from the National Cancer Institute, and a core center grant from the National Institute of Environmental Health Sciences. 

This is a current list of where and when I am scheduled to speak:

• I’m speaking, signing books, and participating in panel discussions at LAcon V in Anaheim, California, USA. My full schedule is here.
• I’m speaking online (via Zoom) at a League of Women Voters event on Tuesday, September 22, 2026, at 5 PM ET.
• I’m speaking at Elevate Festival in Toronto, Canada. The conference runs September 22–24, 2026; my talk is on Wednesday, September 23.
• I’m speaking at CanSecWest 2026 in Vancouver, Canada. The conference runs September 30–October 1, 2026; the time of my talk is TBD...

Epithelial cells are the tiny shields that line and protect our body. In a developing embryo, epithelial cells grow, divide, and move into positions to form the outer layers of our skin and the surfaces of our organs and blood vessels. When we scrape our skin, suffer an internal tear, or undergo surgery, epithelial cells will migrate to the site of injury to heal a wound. And when epithelial cells go haywire, they can turn malignant and spread through the body as cancer. 

MIT engineers have now discovered that as they migrate, epithelial cells can synchronize and collectively pulse. In a study appearing today in the journal Newton, the researchers report observing groups of epithelial cells repeatedly moving in, then out, like a circle of dancers coming together and pulling apart. 

The team measured this collective rhythmic pulsing in different types of epithelial cells, including healthy cells, cells from benign tumors, and cancerous cells. 

Surprisingly, they discovered that malignant epithelial cells were more persistent in their synchronization, pulsing together for twice as long as healthier cells. It’s unclear why the cells sync up in this way. But the researchers suspect that this cellular dance can serve as a clinical signal.

“More aggressive cancer cells tend to have a steadier and more persistent rhythm as compared to healthy ones,” says study author Ming Guo, professor of mechanical engineering at MIT. “We think this coordination could serve as an early warning sign of how likely a tumor is to spread. The same coordinated waves may help shape embryos during development and close wounds upon injury.”

The study includes first author and former MIT graduate student Wenhui Tang SM ’20, PhD ’24; Mehrana Nejad and L. Mahadevan of Harvard University; and Adrian Pegoraro of the Metrology Research Centre of the National Research Council Canada. 

Cells got rhythm

When studying how epithelial cells organize and develop into whole organs and tissues, scientists have focused mainly on how the cells coordinate in space. Where cells move, where they are in relation to the growing tissue, and where they end up, are questions of spatial coordination that scientists including Guo have looked to investigate. How the movement of cells relate over time is less well-understood. 

Guo’s group at MIT studies cell interactions to identify patterns that relate to healthy versus diseased states. As part of this work, the team takes microscopic snapshots of cells that they grow in the lab, to identify interesting behaviors among cells. Recently, Tang, then a member of Guo’s lab, was looking at a series of movies of epithelial cells when she started to see a rhythm, or pattern over time.

“I was studying collective cell migration, and I observed cells were swelling, then squeezing together, then swelling, again and again, forming local patterns,” Tang recalls. “That’s when I realized there might be something more interesting happening with these cells over time.”

Taking a pulse

In their new study, the researchers focused on the timing of cellular movements. They started by studying healthy, live epithelial cells that they cultured in the lab. They stained the cells with fluorescent dye to illuminate each cell’s nucleus. This way, they could easily identify one cell from another. They kept the cells in dishes with nutrients to help them naturally grow, divide, and move about. 

“We’re looking at their natural migration process, related to how they would migrate during different processes in the body, such as when forming skin and organs, and healing wounds,” Guo explains.

Using a confocal microscope, the team took snapshots of the cells every few minutes, for up to 30 hours. When they strung the images together as a sort of movie, a distinct pattern emerged. 

“If you just stare at any one location, you can see those dots are coming together, and then going further away, then coming together again, and going further away, like waves,” Tang says. 

They observed that a single pulse occurred over about an hour. This pulsing persisted in healthy cells, as a slow and steady rhythm over the 30-hour period. 

Curious as to whether other types of epithelial cells would sync up in similar fashion, the team tried the same experiment with several different lines of human breast cancer epithelial cells. They studied the movement of cells from benign tumors and cells of increasing malignancy. They observed similar pockets of synchronized pulsing in every cell type, especially in the most cancerous cells. 

“We found the really dangerous cancer cells team up over time, and do this persistent oscillation, twice as long as healthy cells,” Guo says. “This is unexpected. We see they really team up, synchronize, and oscillate together, which potentially facilitates their invasion.”

The researchers also observed a correlation between cell synchronization, and cell density: In each dish of cells, regardless of type, the cells continued to grow, divide, and pulse. As their numbers grew, more cells pulsed together, and their synchronization increased, up to a point. Once the cells reached a certain density, their pulsing began to die down.

“There’s a peak of synchrony before it decreases as cell density continues to increase,” Tang says.

This connection is especially interesting in the context of certain conditions such as asthma. Epithelial cells line the inside of many organs and tissues, including the airways. In healthy people, these cells pack together and “jam” up to form a solid, stable lining that protects the airways. In asthmatic airways, however, epithelial cells are less able to jam together. This results in airways that are loose and fragile, easily irritated, and difficult to heal. 

Guo and Tang suspect that, as there appears to be a connection between cell density and cell synchronization, there may be a way to target asthma treatments, by watching how potential drugs affect asthma cell synchronization. A similar approach could be taken for the screening of cancer drugs.

“More malignant cells would be better synchronized. After treating them with a drug, if their synchronization is disrupted, then it might be an efficient drug where we can consider the next step,” Guo envisions.

This research was supported, in part, by the National Institutes of Health.

This essay was written with Nathan E. Sanders, and originally appeared in The Guardian.

OpenAI, and then Anthropic, were each formed by AI developers who feared unrestrained corporate AI development—specifically, that companies like Google and Meta would steer the technology towards deleterious, maybe even catastrophically unsafe, outcomes for society. Their founders proclaimed that their new labs, uniquely, could be trusted to develop the technology in humanity’s best interest. But each, in turn, were themselves co-opted by the same market incentives, themselves becoming corporate behemoths zealously guarding future investor value rather than the public interest...

Justice Department lawyers are defending a FEMA program that environmentalists support.

Drivers are buying more electric cars and using less gasoline in plug-in hybrids, the International Energy Agency said.

A strategy outlined this week by Republican Gov. Patrick Morrisey highlights a state law that would steer half the sector’s tax revenue toward reducing and possibly eliminating statewide income taxes.

A Dutch bank published an analysis that estimated heat waves and drought could reduce gross domestic product across the European Union by 1 percent for 2026.

Bolsa Chica and Huntington state beaches reported more than 3,100 incidents so far this year, twice the number for all of 2025.

Dozens of miles of underground water pipes could prove useful beyond the winter months as the risk of wildfires grows.

The initial figures are based on an extrapolation of costs compiled by France’s official statistics agency.

Within the brain, neurons compute by generating electrical impulses. These signals travel throughout neurons, which are in turn connected in vast networks that control brain functions such as sensory perception, memory formation, and control of movement. 

In an advance that could help neuroscientists map those neural networks, leading to a better understanding of how neural activity underlies behavior and other brain functions, MIT engineers have invented a new microscope that can image electrical activity in neurons distributed across the brain of an entire organism, the experimental model Danio rerio (zebrafish).

Using a microscope that they adapted for fast, high-volumetric rate imaging, the researchers were able to track electrical activity across the brain on the scale of milliseconds. This method revealed patterns of neural activity from neurons throughout the brain that were activated in response to ultraviolet light.

“All of the parts of the brain are connected together, so if you want to truly understand the brain, you have to understand how all the neurons work together as an emergent whole,” says Ed Boyden, the Y. Eva Tan Professor in Neurotechnology at MIT; a professor of biological engineering, media arts and sciences, and brain and cognitive sciences; and a member of MIT’s McGovern Institute for Brain Research, Yang Tan Collective, and the Koch Institute for Integrative Cancer Research.

Boyden is the senior author of the study, which appears today in Nature Methods. Former J. Douglas Tan Postdoctoral Fellow Zeguan Wang PhD ’24 and former MIT research scientist Jie Zhang are the lead authors of the paper. Other authors include former MIT postdoc Panagiotis Symvoulidis, Picower Institute research scientist Wei Guo, graduate students Davy Deng and Lige Zhang, Koch Institute research scientist Adam Amsterdam, Picower Institute research scientist Takato Honda, Boston College undergraduate Steven Roche, and Matthew Wilson, the Sherman Fairchild Professor of Neuroscience at MIT and a member of the Picower Institute.

High-speed imaging

One technique often used to measure neuron activity in the brain is calcium imaging. Calcium flows into neurons after they fire an electrical impulse, so measuring calcium levels in the cells can serve as a proxy for neural activity. However, this type of imaging isn’t fast enough to capture single spikes of activity.

“Calcium imaging inherently is very slow, so you’re talking about imaging activity on the order of seconds or even minutes. Typically that is too slow for us to be able to see a lot of these high-speed neural activities,” Zhang says. “Neurons compute using electrical activity, so with voltage imaging, you can get direct observation of that.” 

To enable direct imaging of voltage, researchers have developed proteins called genetically encoded voltage indicators — fluorescent proteins that can be genetically expressed in neurons. When a neuron fires an impulse, the protein fluoresces, which can be detected with a fluorescence microscope.

In previous work, researchers have used these proteins to image small populations of neurons, usually focusing on one localized part of the brain. Until now, there hasn’t been a way to image a large volume, such as the entire brain, with the millisecond-scale resolution needed to see electrical impulses from individual neurons.

To achieve that, the MIT team decided to modify a commonly used microscope known as a light sheet microscope. This type of microscope uses a sheet of laser light to illuminate a thin slice of a sample. By imaging many layers in sequence, this technique can generate 3D images of a large volume. However, with previous microscopes, the scanning of an entire volume would take too long to be able to capture neuronal impulses across the volume at single cell resolution. 

“Different groups of neurons that are distributed across the brain coordinate together at millisecond timescales to generate a lot of behaviors and brain computations,” Wang says. “To understand the principles, we need the technology to observe their activity at the same time, across the whole brain, so we are not missing any important participant neurons.”

To make the imaging process fast enough to image millisecond-scale activity, the researchers increased the image acquisition speed of the microscope’s camera, and they also boosted the scanning speed of the microscope using a technique called remote refocusing.

Using this approach, the researchers showed that they could scan the entire zebrafish brain 200 times per second, or once every five milliseconds. 

Mapping brain activity

To test the new microscope, the researchers engineered neurons in larval zebrafish to express a voltage indicator called Positron2-Kv. Although they had hoped that the indicator would end up in every neuron, it produced signals in neurons distributed throughout the brain, with about one quarter of the neurons exhibiting acceptable signals. This was enough, however, to observe patterns of activity across the brain. The researchers imaged the brain as the fish were resting, and they were able to observe single voltage spikes from neurons, as well as rapid bursts of spikes.

Additionally, this technique revealed patterns in how the brain is activated following a stimulus such as ultraviolet light. Immediately following the stimulus, activity was seen in the optic tectum, which receives and processes visual input from the retina. This activity propagated from one side of a part of the brain called the tectum to the other. Stimulus-independent activity also occurred in sequences across sets of neurons in the cerebellum and hindbrain.

The researchers now hope to increase the percentage of neurons that they can image across the brain, as well as the microscope’s speed and resolution. They are also working on expanding the use of this technique to other experimental models, including mice.

This approach, they say, could offer neuroscientists a new way to generate hypotheses about what happens in the brain when it engages in specific behaviors, or about how brain activity is linked to states of mind such as daydreaming.

“A big question is simply to understand how neurons work together as a network. And this might be the first time that you could do that, because you can image the voltage of neurons distributed throughout the network,” Boyden says.

The research was funded by the National Institutes of Health, the BRAIN Initiative, the Picower Institute Innovation Fund, K. Lisa Yang, Ashar Aziz, the K. Lisa Yang and Hock E. Tan Center for Molecular Therapeutics in Neuroscience at MIT, the Hock E. Tan and K. Lisa Yang Center for Autism Research, the Alana Down Syndrome Center, John Doerr, Jed McCaleb, James Fickel, and the Howard Hughes Medical Institute.

Nature Climate Change, Published online: 14 August 2026; doi:10.1038/s41558-026-02691-0

Although many cities have set net-zero targets, there is limited understanding of their residual emissions strategies. An analysis of 103 European cities reveals best practices but also a potential over-reliance on temporary land-based carbon removal and the limited robustness of compensation strategies.

Flock Safety, the embattled vendor of mass surveillance technology, has rolled out a handful of new reforms intended to appease the justified nationwide anger that has seen scores of towns cancel or suspend their contracts with the company for automated license plate readers (ALPRs). The reforms are a combination of long overdue changes along with some cosmetic fixes that fail to address the fundamental dangers of this technology.  

We should not be letting companies decide how much privacy we deserve.

So, what do these reforms actually do?  

The most consequential is Flock’s default setting of an optional 7-day retention period for ALPR data, down from its original default optional 30-day retention period. This means if police want to retain data beyond the duration of their retention setting, they need to access “Evidence Mode,” i.e., when the desired data is associated with an active investigation and not just a fishing expedition. This is significant because, in at least some circumstances, Flock has previously charged its customers to extend their retention period. So, while towns can likely easily flip the switch to longer retention periods, it might come with a price tag some cities will be unwilling to pay.  

Flock also has two other, likely easier-to-bypass reforms. The first is offense filtering so that cities can enable other departments to access their ALPR data only if they are investigating certain crimes, e.g., murder or robbery but not immigration-related investigations. The second is supposedly beefing up their audit feature and proactively locking out officers who file suspicious requests for data. The major problem here is the fact that Flock’s enhanced audit and transparency tools help to address a problem that Flock itself has created—an abusable mass surveillance system that tracks all cars all the time.  

In addition to these reforms, there is also a tone shift coming from Flock’s CEO, Garrett Langley. Langley went from calling the DeFlock movement “terrorists” (which he has since apologized for) and saying that the wave of anti-surveillance anger was more about the current federal administration than it was specifically about his company, to a more conciliatory tone that acknowledges some of the problems of dangerous surveillance, mission creep, and police abuse.  Just look at this report from the BBC:  

“Historically, my point of view as a chief executive of a private company was, I don't know if I should be making these decisions. I don't know if it's my job to say how long data should be retained,” Langley said. 

He added that he has come to agree with groups like the American Civil Liberties Union and the Electronic Frontier Foundation that police should need an active case number to search Flock's data. 

“They're right. I think it should be required.” 

To be clear, our position has long been that police, at a minimum, need to get a warrant, signed by a judge, in order to search for historic ALPR data regarding specific vehicles. For us, it’s common sense: if police want to dip into historic ALPR data like they were going back in time to retroactively follow your comings and goings, they need a warrant.  

Fundamentally, these reforms leave us wondering: what is stopping Flock from reversing course on them if their law enforcement customers respond by defecting to another ALPR vendor? Nothing.  

This all leads to the bigger and more important issue: We should not be letting companies decide how much privacy we deserve. If our privacy is determined by how much surveillance technology vendors decide is too much surveillance, then we’re really out of luck. It shouldn’t be up Flock or any other ALPR vendor to decide how long police can collect and retain data on millions, if not hundreds of millions, of innocent people. We need lawmakers to step up and pass laws that restrict police’s use of surveillance technology. After all, the surveillance business model is the problem, and a few company-imposed slapdash reforms aren’t going to change that.

Related Cases: SIREN and CAIR-CA v. San Jose

This essay was written with Nathan E. Sanders, and originally appeared in Tech Policy Press.

AI represents the first time we humans can do cognitive work outside of our bodies at scale. The only comparable moment is the early years of the industrial revolution, when new technologies like the steam engine provided a quantum leap in our ability to do mechanical work outside of our bodies at scale. If AI’s cognitive capabilities become integrated into our lives, businesses, and governments—a process that will take years if not decades—society will be as unrecognizable as the modern world would be to a preindustrial farmer. And yet, Americans—by a wide margin—...

Property insurers show “where their loyalties lie” in urging court to block climate lawsuits against oil and gas industry, environmentalists say.

Exxon and other fossil fuel producers told a court Tuesday that a lawsuit by the island's towns should have been filed within four years of Hurricane Maria.

The Democratic front-runner in the governor’s race has raised doubts about the state’s ambitious climate goals.