Others have shown that extended exposure of β-cells to glibenclamide, an ATP-sensitive K+-channel inhibitor, which depolarizes the β-cells and thereby stimulates the cells to secrete insulin (often enlisted as a treatment tool for diabetes) [51], causes a prolonged increase in the cells’ basal insulin production, and showed that this was a Ca2+-dependent effect [52]. The gene discussed is INS; the disease is diabetes mellitus.