It is believed that this mTORC2 inhibitory action, which perpetuated a decrease in IRS degradation, AKT activation and mTORC2-induced insulin receptor signaling, is partially responsible for rapamycin-induced hyperinsulinemia, IR and diabetes-like syndrome after its chronic usage (Deblon et al., 2012; Lamming et al., 2012; Martina et al., 2012). This evidence concerns the gene AKT1 and hyperinsulinism.