Regarding KATP channel-activating mutations, they either impair ATP binding to the channel Kir6.2 mutant and is impaired or enhanced by the binding of Mg-nucleotide to SUR1 mutant leading to KATP channel opening, membrane hyperpolarization, impaired insulin release, and can lead to NDM [59]. This evidence concerns the gene KCNJ11 and neonatal diabetes mellitus.