Observations that aspirin somehow thwarts cancer have subsisted for decades, but we are just beginning to understand how. This review unpacks new mechanistic data revealing low-dose aspirin may prevent metastasis by disarming platelet-mediated immune suppression. Aspirin irreversibly inhibits platelet COX-1, shutting down platelet-derived thromboxane A₂ (TXA₂) production for the platelet’s lifespan. TXA₂ is an important down-regulator of T-cell activation, thus aspirin’s blunting of TXA₂ restores T cell-mediated micrometastasis elimination. In mouse models, aspirin reduced metastases—but only when TXA₂-mediated signaling in T cells was intact—firmly linking aspirin’s antimetastatic effect to adaptive immunity rather than generic anti-inflammation. This is the cleanest biologic explanation yet for aspirin’s anticancer effects—and it points squarely at platelets as accomplices in immune escape. | Langley, N Engl J Med 2025 & Yang, Nature 2025
