During the progression of T2DM, Adenosine 5’-monophosphate (AMP)-activated protein kinase (AMPK) is inactivated, leading to a chronic overactivation of mechanistic target of rapamycin (mTOR) C1 (45), which has been associated with insulin resistance and progression of diabetes-induced complications (46). This evidence concerns the gene MTOR and type 2 diabetes mellitus.