A reduction in endothelium-derived NO bioavailability has been suggested to be responsible for endothelial dysfunction in patients with hypertension for the following two possible reasons: 1) decreased NO production by endothelial nitric oxide synthase (eNOS) 9; and 2) increased levels of vascular superoxide, which increase NO degradation 5. The gene discussed is NOS3; the disease is endothelial dysfunction.