INS and hyperinsulinism: Initially believed to result from dysfunctional pancreatic β cell-specific KATP channels that are typically activated in response to low glucose levels to hyperpolarize pancreatic β cells and prevent basal insulin secretion,61 our results were not able to support this hypothesis, as the Kir6.2 KO mice did not exhibit hyperinsulinemia after prolonged fasting (Figure 4D and Supplementary Table S3).