CD38 KO mice did not show insulin resistance, suggesting that the observed phenotype is indeed caused by the absence of CD38 in pancreatic β-cells.91) The KO islets, however, responded normally to the extracellular Ca2+ influx stimulants tolbutamide and KCl to secrete insulin.91) Thus, as shown in Fig. 6, the CD38-cADPR signal system as well as the ATP-sensitive K+ channel system appeared to function almost equally in insulin secretion by glucose stimulation. The gene discussed is CD38; the disease is Insulin resistance.