Insulin unable to supress clearance of FFAs and lipolysis in adipocytes, creates a constant negative feedback loop.8 This progressive loss of insulin sensitivity leads to hyperglycemia, promoting demand for pancreatic β-cells to expand, produce and secrete more insulin as a compensatory mechanism.9 The hyperinsulinemia response by β-cells initially restores plasma glucose levels in the prediabetic stage. This evidence concerns the gene INS and Hyperinsulinemia.