Introducing a genetic deletion of NOX1 in leptin receptor-deficient db/db mice restored endothelial function, myogenic tone, and NO-dependent vascular regulation in mesenteric resistance arteries.20 Our study expands the role of NOX1 in metabolic disease from the peripheral to the myocardial vasculature, and from atherosclerosis and hypertension to the clinical entity of metabolic heart disease. The gene discussed is LEPR; the disease is hypertensive disorder.