Mutations in Kir6.2 tend to cause more severe phenotypes of NDM than those in SUR1, and the hyperactivity of the resulting mutant KATP channels is less likely to be adequately suppressed by sulfonylureas (Hattersley and Ashcroft, 2005; Pipatpolkai et al., 2020). This evidence concerns the gene KCNJ11 and neonatal diabetes mellitus.