The defect in alpha-cell function that occurs in T2DM reflects deranged glucose sensing by these cells.[7] Moreover, absence of proper beta-cell suppression of alpha-cell secretion has been invoked as a mechanism that clarifies exaggerated glucagon responses, especially common in patients with deficient beta-cell secretion (T1DM and insulinopenic T2DM).[8] From these facts, it can be concluded that by using exogenous insulin and/or by reducing glucagon level, blood glucose concentration may be controlled. This evidence concerns the gene INS and type 1 diabetes mellitus.