Statin inhibits HMG CoA reductase in cholesterol biosynthesis and lowers cholesterol levels in blood. It has been established by a lot of clinical studies that statin has protective effects against cardiovascular diseases. Experimental studies have shown that statin inhibits membrane translocation of Rho and Ras GTPases that results in activation, by decreasing cellular levels of isoprenoid intermediates. Inhibition of Rho by statin increases VEGF expression in endothelial cells that promotes cell survival. Statin also prevents endothelial hyperpermeability that is implicated in atherogenesis. Ras-mediated activation of T type calcium channel that may result in endothelial cell dysfunction is blocked by statin. Accordingly, statin has pleiotropic effects on cardiovascular cell function by modulating cell signaling.