Rapamycin's ability to inhibit hepatic mTORC2 may explain why it causes glucose intolerance because mice lacking hepatic Rictor but not Raptor are glucose intolerant52; however, hepatic Rictor-deficient mice have relatively normal insulin sensitivity indicating unknown extra-hepatic target(s) likely contribute to rapamycin-induced metabolic syndrome. This evidence concerns the gene RICTOR and metabolic syndrome.