A long way has been travelled since platelets were likened to sponges in 1961. At that time research on thrombotic mechanisms was mainly concentrated on blood coagulation. Since then, a shift of emphasis toward the study of platelets has dramatically evolved. How to prevent platelets from becoming sticky at sites of injury has been the main concern for platelet researchers over the past decade. Following adherence of platelets to a damaged vessel wall, prostaglandin synthesis is triggered leading to the formation of thromboxane A2, the most potent platelet activating agent so far discovered. By an "autocatalytic" process, thromboxane A2 together with the released ADP are responsible for the growth of the platelet thrombus. Among the substances released by the alpha-granules is the mitogenic factor, which, by stimulating the proliferation of smooth muscle cells from the media to intimal layers in arteries, is instrumental in the generation of atherosclerotic plaques. The narrowing of the vessel wall lumen can be further aggravated by the formation of a thrombus over the plaque, thereby occluding the vessel, and leading to cardiovascular diseases or stroke depending on the location of the lesion. An all-out effort to find a means for preventing platelet stickiness is currently under way. The recent discovery of prostacyclin has been the cornerstone for most of the research carried out so far in this field. The presently available antiplatelet drugs should be used with caution. Indeed, whereas a dramatic thrombosis may occur with full platelet activation, a catastrophic hemorrhage may follow the "neutralization" of platelets. Eskimos who are fed with eicosapentaenoic acid, the precursor of a potent antiplatelet agent, may indeed be immune against thrombotic disorders; however, they have an increased tendency to bleed.