Generally injuries that remove or disrupt the endothelial cells lining blood vessels stimulate formation of vascular lesions composed of smooth muscle cells. One of the first events after such endothelial cell disruption is the generation of thrombin at the site of injury. This leads to platelet activation and thrombus formation. Evidence suggests that thrombus formation may stimulate smooth muscle-cell proliferation through the action of any number of factors emanating from the thrombus including platelet- or macrophage-derived factors, platelet-derived growth factor, basic fibroblast growth factor or thrombin. Atherosclerotic plaques continue to grow for many years. The slow indolent process of nondenuding chemical injury of the endothelium and lesion formation may be accelerated periodically by thrombi forming on the lumenal surface at sites of small denuding injuries leading to progressive atherosclerotic disease. Genistein, an isoflavonoid derived from soy products, has been shown to inhibit thrombin formation and platelet activation in vitro in addition to its antigrowth factor activity. Should it have similar actions in vivo, this compound has the potential to affect the progression of atherosclerotic disease by modifying coagulation responses. To assess the potential of genistein as a therapeutic for vascular disease, additional studies will be required to establish its effect on experimental vascular lesion formation.