The discrepant findings of elevated miR-192 and miR194 in akt2−/− mice but no alteration in HFD fed E3L*CETP mice may hence reflect the different pathogenesis of hyperglycemia in these mice: The lack of Akt2 causes insulin resistance however without promoting lipogenesis, steatosis and dyslipidemia, because some lipogenic effects of insulin involve signaling via Akt246. The gene discussed is AKT2; the disease is Insulin resistance.