Vascular inflammation and its subsequent endothelial dysfunction play a fundamental role in the initiation and progression of atherosclerosis. Accumulating evidence shows that various pro-inflammatory cytokines including tumor necrosis factor (TNF)-a, interleukin 1 beta (IL-1ß) and interferon (INF)-? are critically involved in the pathogenesis of atherosclerosis. An elevated blood level of these pro-inflammatory mediators is validated markers of vascular inflammation, which can subsequently lead to the development of atherosclerosis. The overall objective of this project is to evaluate the cellular mechanism(s) of action of genistein in its protective effect against cytokine-induced vascular dysfunction.