Our results showed that insulin resistance exhibited by HFD-fed Apoe−/− mice in the ITT experiments could be due to an impairment in AKT phosphorylation (Thr308) because we did not observe an increase in the phosphorylation of this residue after insulin stimulation, hindering the full activation of this kinase (Fig. 4D). The gene discussed is AKT1; the disease is Insulin resistance.