No similar parental studies were possible for P2; however, this finding raises the possibility that, in P1, progressive obesity has led to a state of insulin resistance determined by inherited, presumably oligogenic factors and that this is exerted at or beyond the level of AKT2 in liver and adipose tissue, effectively attenuating the basal AKT activation that was driving hypoglycemia and free fatty acid suppression. The gene discussed is AKT1; the disease is Obesity.