Endothelial dysfunction is the initial step in the pathogenesis of atherosclerosis and is characterized by decreased bioavailability of nitric oxide (NO), which may be due to enhanced NO catabolism secondary to increased superoxide anion (O2●−) production or reduced expression and/or activity of endothelial nitric oxide synthase (eNOS) [13,14,15]. The gene discussed is NOS3; the disease is atherosclerosis.