The most common alterations in insulin resistance include a reduction in the number of insulin receptors and their catalytic activity, increased Ser/Thr phosphorylation of the insulin receptor and IRS, elevated tyrosine phosphatase activity—primarily of protein tyrosine phosphatase 1B (PTP-1B), which dephosphorylates the receptor and IRS—and decreased activity of phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), and mammalian target of rapamycin (mTOR), crucial for muscle contractile protein synthesis. This evidence concerns the gene AKT1 and Insulin resistance.