In the prediabetic condition, insulin fails to trigger a response in insulin-dependent tissues, such as the skeletal muscle; as a result, the accumulation of glucose in circulation promotes glycation with hemoglobin, which then causes the β-cells of the pancreas to react by producing more insulin in order to control the rise in blood glucose levels, leading to compensatory hyperinsulinemia [39,40]. Here, INS is linked to hyperinsulinism.