A recent study demonstrates that SESN2 ablation exacerbates obesity-induced mTORC1-S6K activation, glucose intolerance, insulin resistance, and hepatosteatosis; all of which are reversed by AMPK activation, suggesting that SESN2 exerts in addition to important homeostatic functions in the control of mammalian lipid and glucose metabolism (Lee et al. 2012a). This evidence concerns the gene RPS6KB1 and Glucose intolerance.