SU drug promotes insulin secretion by acting on pancreatic β cell. The hypoglycemic effect is the most powerful among oral diabetic drugs with high cost-effectiveness. Particularly for the Japanese with type 2 diabetes caused by a decrease in insulin secretion as a main pathological condition, it was widely used until the present since 1957 and largely contributed for the sickness. On the other hand, it is true that a number of issues such as a prolonged hypoglycemic coma or obesity due to a neglect of proper usage, patient education, and a possibility of second failure have been discussed so far. After a structure of K(ATP) channel on pancreatic β cell as playing an important role with insulin secretion is clarified recently and neonatal diabetes mellitus by the genetic defect is reported, a new possibility for SU drug receives attention. Furthermore, a receptor of SU drug on β cell membrane was solely known as a target molecule for SU drug, but since a binding to Epac2 as a protein to detect a part of SU drug's cAMP signal within β cell is determined, a relation with an enhancing mechanism of insulin secretion by incretin is being clarified at present. As understanding a new potential for SU drug, we consider a positioning and proper usage for SU drug again.