Sodium–glucose cotransporter 2 inhibitors (SGLT2is) were originally developed for the treatment of type 2 diabetes mellitus (T2DM), and their glucose-lowering mechanism does not depend on improving insulin secretion or resistance, rather they block the improving insulin secretion or resistance as well as exert their glucose-lowering effects by blocking glucose reabsorption from the proximal renal tubule, thus increasing urinary glucose excretion. This evidence concerns the gene INS and diabetes mellitus.