Mounting evidence implicates β-cell dysfunction as the primary cause associated with the progression of T2DM, and defective early phase insulin release has been clearly demonstrated in patients with the disease.[16] There are many antidiabetic agents with different mechanisms; however, a number of patients with diabetes have experienced frustrations from poor glycemic control despite adherence.[17] There is an urgent need for clinically differentiated oral antidiabetic agents to address drivers of β-cell dysfunction and improve the function of the defective glucose sensor. This evidence concerns the gene INS and diabetes mellitus.