The presence of metabolic dyslipidemia and fatty liver in those with AKT2 mutations but not in those with an insulin receptor mutation suggests that the pathway required for hyperinsulinemia to drive liver fat accumulation and atherogenic very low-density lipoprotein (VLDL) secretion depends on the insulin receptor but not on AKT2. The gene discussed is AKT2; the disease is Hyperinsulinemia.