Remarkably, in the above-described obesity models, inhibitors of hepatic aPKC (used in doses that only partially reduce hepatic aPKC activity) fully or largely restore: (a) the impairment in hepatic Akt-dependent FoxO1 phosphorylation; (b) excessive hepatic expression of gluconeogenic enzymes, PEPCK and G6Pase; and (c) insulin signaling to both Akt and aPKC in muscle [13,18]. The gene discussed is AKT1; the disease is obesity disorder.