Several factors contribute to this increased SNS activation: baroreceptor reflex impairment (impairment of baroreceptor control on sympathetic nerve activity) [20]; hyperinsulinemia (insulin activates the SNS directly through hypothalamic action) [21]; angiotensin II, along with other RAAS metabolites, contributes to increased SNS activation; cytokine release from adipocytes, especially leptin, is a key contributor, which will be detailed below; and the pro-opiomelanocortin (POMC) pathway. The gene discussed is AGT; the disease is hyperinsulinism.