Vav plays a key role in modulating platelet activation. Hyperlipidemia leads to increased plasma levels of oxidized LDL (oxLDL). OxLDL interacts with the scavenger receptor CD36 on the surface of platelets, triggering an intracellular signaling pathway. The Src kinase Fyn phosphorylates Vav isoforms, which in turn increase the sensitivity of platelets to activation. Vav thus provides a mechanistic link between hyperlipidemia and thrombosis. Professional illustration by Kenneth X. Probst.