Circulating platelets are activated by newly exposed collagen fibrils and locally generated thrombin at sites of vascular injury. Using von Willebrand factor as a cofactor, platelets adhere to the vessel wall, spreading out and forming a monolayer. Additional platelets are recruited through the continued action of thrombin, as well as the release of soluble molecules such as ADP and thromboxane A2 (TxA₂). As more platelets become activated, they stick to each other (cohesion), increasing the height of the thrombus. ADP supports all of these events by binding to G protein–coupled receptors on the platelet surface. The studies of Cosemans et al show that ADP is also needed for thrombus stability, helping to protect it from premature dissolution. Illustration by Kenneth Probst.