To summarize, it seems clear that excessive activity of hepatic aPKC plays a key role in promoting systemic insulin resistance in HFF17, 20, 40, 41, 42, 43 and ob/ob21, 40, 41 mice and in producing a “T2DM enzymatic phenotype” in livers of these mice and livers of obese and T2DM humans,18, 19, 43 wherein insulin signaling is deficient to Akt and excessive to aPKC, and, moreover, is accompanied by increases in expression of gluconeogenic, lipogenic, and proinflammatory enzymes. The gene discussed is AKT1; the disease is type 2 diabetes mellitus.