The β-cell dysfunction is initially characterized by impairment in the first phase of insulin secretion following glucose stimulation, resulting in impaired glucose tolerance (a prediabetic state) and postprandial hyperglycemia.[1–3] As the disease progresses, the second phase secretion declines, resulting in fasting hyperglycemia, i.e., either impaired fasting glucose (IFG) or T2DM.[4] This β-cell dysfunction is thought to be progressive and irreversible. Here, INS is linked to type 2 diabetes mellitus.