Numerous stimuli promote sustained activation of vascular Nox including several growth factors (platelet-derived growth factor (PDGF) [47], epidermal growth factor (EGF) [48], and TGF-β1 [49]), cytokines [50], mechanical forces (cyclic stretch, laminar, and oscillatory shear stress) [51], metabolic factors (hyperglycemia, hyperinsulinemia, free fatty acids, and advanced glycation end products) [52], and G protein–coupled receptor agonists (serotonin, thrombin, bradykinin, endothelin, and angiotensin II [Ang II]) [53]. The gene discussed is AGT; the disease is hyperinsulinism.