In the above scenario, hyperinsulinemia can indeed provoke adverse responses, including increases in hepatic lipogenesis that contribute to hypertriglyceridemia, hypercholesterolemia, hepatosteatosis, and extrahepatic fat deposition, that is, obesity; increases in renal release of renin and resultant angiotensin‐mediated vasoconstriction and aldosterone‐mediated sodium retention; increases in tumor/cancer growth; and increases in neuronal BACE1, which abets Alzheimer development. The gene discussed is BACE1; the disease is hyperinsulinism.