The most prevalent changes in insulin resistance include (1) a reduction in the number of insulin receptors and their catalytic activities; (2) enhanced Ser/Thr phosphorylation in the insulin receptors and IRS; (3) enhanced Tyr phosphatase activity, in particular PTP-1B involving receptors and IRS dephosphorylation; (4) lowered PI3K and AKT kinase activity; and (5) defects in functions and expression of GLUT4 [25]. This evidence concerns the gene INSR and Insulin resistance.