Plasma levels of AnxA1 are reduced in stroke, and AnxA1 can act on human platelets, thereby inhibiting the classic thrombin-induced internal-outside signaling events; for example, Akt activation, intracellular calcium release, and Ras-related protein 1 (Rap1) expression reduce αβ activation without changing its surface expression [58]. This evidence concerns the gene ANXA1 and Stroke.