Compared with nondiabetic people, the number of islet β cells is reduced by ≈50% in T2DM patients.[6] Currently, >10 classes of drugs have been approved for T2DM treatment, such as biguanides, sulfonylureas, meglitinides, amylin mimetics, glucagon‐like peptide‐1 analogs, and insulin.[7] These drugs have contributed to dramatic improvements in the quality of diabetes care and self‐care in recent years, but there are still no drugs for the underlying pathological process leading to the destruction of islet β cells, which is what ultimately leads to the onset and progression of T2DM.[8]. The gene discussed is INS; the disease is type 2 diabetes mellitus.