Recently, accumulating evidence has revealed that pancreatic β-cell dysfunctions including glucose-stimulated insulin secretion (GSIS) defect and β-cell mass loss are major determinants for the progression from prediabetes with normoglycemia to diabetes with hyperglycemia, and the result that insulin resistance in prediabetes needs compensatory insulin hypersecretion likely leads to a progressive decline in islet β-cell function.2 Therefore, an ideal strategy for T2DM treatment is to improve pancreatic β-cell function.1, 2. This evidence concerns the gene INS and prediabetes syndrome.