Peter Attia· MD
So you needed SARC for middle T to bind to PI3 kinase.
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The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
So you needed SARC for middle T to bind to PI3 kinase.
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
And even more importantly, that if you mutated that tyrosine residue to phenylalanine, polyamimidal T completely lost its ability to transform cells. It's a single point mutation. Even though the Sark protein was still bound, there was no longer tyrosine phosphorylation 315, and that eliminated the ability to transform cells.
We already knew by the mid-70s that SARC was somehow implicated in how polyomimidal T transforms cells and forms all these tumors.
Whole-body MRI screening in healthy adults produces more incidentaloma harm than cancer-mortality benefit.
Starting colonoscopy screening at 45 (vs 50) prevents enough early-onset cancers to justify the population cost.
Multi-cancer liquid-biopsy tests like Galleri detect early cancers at a stage that meaningfully improves survival.