Altered platelet function reported in diabetic patients appears to be involved in the pathogenesis of diabetic vascular complications. However until recently, the role of platelets in progression of spontaneous atherosclerosis remained questionable. The original version of the response to injury hypothesis, where deposited platelets at denuded endothelium play key roles in the spontaneous development of atherosclerosis, has been modified dramatically over the past three decades; atherogenesis is now considered a chronic inflammatory process in which monocytes and T cells play central roles. Recently however, evidence has been accumulated that activated platelet contributes to progression of atherosclerosis in apo E-deficient mice. Activated platelets aggregate with leukocytes, release proinflammatory cytokines, chemokines and growth regulatory molecules, resulting in endothelial activation, leukocyte recruitment and altered smooth muscle cell function. Indeed, it has been shown that activated platelets, and their aggregates with leukocytes are found in the circulation of patients with coronary artery diseases. We have recently shown that circulating P-selectin positive platelets, which are higher in diabetic patients than non-diabetic subjects, are significantly and positively associated with carotid atherosclerosis in the large-scale human studies. This review will focus on altered platelet function in diabetic patients, and its implications in the progression of atherosclerosis.