Blood coagulation is initiated following injury to the blood vessel wall through the exposure of tissue factor, which mediates the activation of circulating factor VII. Activated factor VIIa forms a complex with tissue factor and triggers the subsequent steps in the activation of the coagulation system, ultimately culminating in the conversion of prothrombin to thrombin (1, 2, 3, 4, 5). The platelet membrane surface is crucial for this process, providing a milieu, referred to as the prothrombinase complex, for efficient assembly of the coagulation complexes and localization of the procoagulant response. Indeed, recent data have even implicated platelets in the initiation of coagulation as they acquire circulating forms of tissue factor, generated from other cells, on their surface (6,7). Thrombin mediates fibrin formation and plays a critical role in the inflammatory responses (8); thus, the regulation of prothrombin activation by the platelet membrane has broad physiological and pathophysiological implications.