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Yann LeCun reportedly leaving Meta to launch new AI startup

How AI solved a 25-year Crohn's disease mystery

In today’s email:

  • 📈 SoftBank’s Nvidia sale rattles market, raises questions

  • 🎙️ Matthew McConaughey, Michael Caine Ink Deals for AI-Generated versions of Their Voices

  • ☠️ Contacted by the US Secret Service & the AI Surveillance Center Dystopia

  • 🧰 10 new AI-powered tools and resources. Make sure to check the online version for the full list of tools.

Top News

Key Takeaway: FT reports that Yann LeCun is preparing to leave Meta to found a startup likely built on his JEPA vision, after months of internal friction over research controls, org shifts, and disagreement with the LLM-first playbook.

More Insights:

  • Early investor talks underway; no official comment from Meta or LeCun; his NYU post stays.

  • Frustration cited over stricter internal publication reviews seen as curbing academic freedom.

  • FAIR’s influence reportedly waned amid layoffs and a shift to a product-led lab; LeCun was said to report into it.

  • He’s publicly distanced himself from Llama models and has long criticized LLM-centric AI as overhyped.

  • New venture is expected to pursue JEPA: world-model learning focused on prediction, reasoning, and planning over text generation.

Why it matters: If a Turing winner walks away from Big Tech to bet on non-LLM architectures, it signals a real pivot point—capital and talent may flow into alternative paths, accelerating progress toward agents that understand and plan in the world rather than just autocomplete it.

They check in when you forget. They remember what you said you'd do. They take initiative and act autonomously: send emails, manage tasks, and coordinate for you. They see your face in real time, read your body language and tone, and understand your emotions. Move naturally between text, phone calls, and face-to-face video. One continuous conversation. For the first time, AI that works for you instead of the other way around. Proactive. Emotional. Alive. This is what AI was always supposed to be.

Key Takeaway: SoftBank’s Masayoshi Son sold the firm’s entire $5.8B Nvidia stake—about 32.1M shares—likely near peak levels to re-deploy billions into an all-in AI strategy, jolting markets and reviving questions about his high-conviction style.

More Insights:

  • Sale spooked traders: Nvidia fell ~3% after the disclosure despite analysts saying it isn’t a bearish call on the company.

  • Proceeds are earmarked for AI: a planned $30B commitment to OpenAI and hopes to join a proposed $1T AI manufacturing hub in Arizona.

  • Second full Nvidia exit: unlike the ill-timed 2019 sale (shares that’d be >$150B today), this one came ~14% below NVDA’s all-time high.

  • Son’s boom-bust cadence: from a $70B dot-com loss to a $20M Alibaba bet worth ~$150B by 2020.

  • Risk tolerance on display: Vision Fund’s Saudi backing and the costly WeWork saga ($11.5B equity + $2.2B debt losses) underscore his appetite for outsized bets.

Why it matters: If Son is right, the next leg of value won’t be in AI winners like Nvidia’s stock but in owning and building the AI infrastructure and models themselves; if he’s wrong, it’s another late-cycle swing—either way, his move signals capital rushing from chip exposure to full-stack AI bets, a shift that could reshape who captures the next decade of tech profits.

Key Takeaway: UC San Diego scientists used AI plus lab and mouse studies to show that NOD2 must bind girdin to steer macrophages toward healing; common Crohn’s mutations break this link, tipping the gut into chronic inflammation.

More Insights:

  • AI parsed thousands of samples to define a 53-gene macrophage signature separating inflammatory from tissue-repairing cells.

  • NOD2’s specific region binds girdin in noninflammatory macrophages, suppressing runaway inflammation and clearing microbes.

  • The most common Crohn’s-risk NOD2 mutation deletes the girdin-binding section, derailing macrophage balance.

  • Girdin-deficient mice developed dysbiosis, small-intestinal inflammation, and often fatal sepsis, confirming causality.

  • The work resolves a decades-long debate over how the first Crohn’s gene actually drives disease.

Why it matters: If Crohn’s stems from a broken NOD2–girdin handshake, future therapies can move beyond blanket immunosuppression to precisely “retrain” macrophages and restore balance—turning a 25-year mystery into a targeted path for treatment.

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