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. Here, AKT2 is linked to metabolic syndrome.