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. This evidence concerns the gene AKT1 and obesity disorder.