Insulin resistance [5] is one critical process to the development of T2D, which means the function of pancreatic β-cells is commonly normal and insulin secretion is sufficient, but the insulin receptors are insensitive to insulin levels and the ability to stimulate glucose utilization is decreasing, or impairments in insulin signal transduction, resulting in a compensatory hyperinsulinemia [6]. The gene discussed is INS; the disease is hyperinsulinism.