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. The gene discussed is RICTOR; the disease is Glucose intolerance.