Nitric Oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a key mediator of vascular homeostasis, and NO bioavailability is reduced early in vascular disease states such as hypercholesterolemia, diabetes and hypertension, as well as throughout the progression of atherosclerosis1–3. The gene discussed is NOS3; the disease is familial hypercholesterolemia.