The lack of any defect in phosphorylation of the mTORC2 targets AKT T450 and S473 in rictor+/− mice, combined with our data demonstrating that both male and female L-RKO mice develop glucose intolerance while rictor+/− mice of both sexes remain glucose tolerant (Fig. 4), suggests that the sexually dimorphic effect of RICTOR depletion upon lifespan in L-RKO mice is likely not mediated by the activity of mTORC2 toward AKT in the liver, or by the development of hepatic insulin resistance. Here, AKT1 is linked to Insulin resistance.