This is striking contrast to the phenotype of hepatic mTORC2-deficient (and thus Akt Ser473 phosphorylation-incompetent) L-Rictor mice21, which fail to maximally activate Akt, leading to unchecked hepatic glucose output and glucose intolerance, closely approximating ‘complete' hepatic insulin resistance43, 44. This evidence concerns the gene AKT1 and Glucose intolerance.