To recapitulate, and, as will be discussed in greater detail below, with diet-induced excessive activation of hepatic aPKC, there is at first (presumably reflecting an early phase of obesity), an impairment in the ability of Akt to regulate (phosphorylate) downstream factors that diminish gluconeogenesis, and subsequent development of glucose intolerance, insulin resistance, hyperinsulinemia and increases in hepatic production of lipids and proinflammatory factors. The gene discussed is AKT1; the disease is obesity disorder.