Mounting evidence implicates β-cell dysfunction as the primary defect associated with the progression of T2DM, and defective early phase insulin release has been clearly demonstrated in T2DM.[14] Many diabetes patients have experienced frustrations from poor glycemic control despite adherence.[15] There is still an urgent need for clinically differentiated oral antidiabetic agents to address drivers of β-cell dysfunction and repair the defective glucose sensor function. The gene discussed is INS; the disease is type 2 diabetes mellitus.