Absence of mTOR in knockout mice models showed glucose intolerance and insulin resistance characterized by reduced glucose uptake in the muscle and reduced glycogen and lipid deposition in the liver under high fat diet condition (Guridi et al., 2016) while hyperactivation or sustained activation of mTOR has may contribute to hyperglycemia and insulin resistance via inhibition of insulin-induced Protein kinase B (AKT) phosphorylation, blocking glucose uptake in skeletal muscles (Williamson et al., 2015). This evidence concerns the gene AKT1 and Insulin resistance.