Uncoupled eNOS leads to decreased NO production by endothelial cells, but also potentiates oxidative stress in the vasculature, which promotes atherosclerosis.40 In diabetic settings, the uncoupling of eNOS and resultant superoxide production is well documented leading to impaired vascular repair and atherosclerosis, an effect that is rescued with the administration of NO stimulating peptides.41 The gene discussed is NOS3; the disease is atherosclerosis.