Platelets play a dual role in the normal hemostatic process. Injury of a vessel wall causes exposure of structural elements such as collagen that will trap platelets circulating in the blood. This initiates two processes, which occur simultaneously, resulting in formation of a stable thrombus. Adhesion and subsequent activation of platelets, achieved through various ligand-receptor interactions, will cause platelets to clump at the site of injury, thus forming a physical barrier to prevent further blood loss. The primary platelet aggregate thus formed is consolidated by a network of fibrin, the end product of blood coagulation. The latter process involves a cascade of enzymatic reactions, several of which are localized on and strongly enhanced by the presence of a suitable phospholipid surface. This procoagulant phospholipid surface is provided mainly by platelets activated in such a way as to expose anionic phospholipids, in particular phosphatidylserine (PS) (1,2). The thrombin that is produced as a result of the coagulation process is also a potent platelet-activating agonist. Accordingly, it is widely recognized that the processes of platelet activation and coagulation are strongly interacting and mutually dependent (3).