Some SUR1 mutations resulted in increased channel activity in MgATP/MgADP and drastically reduced KATP channel surface expression, which suggests that the overactive defects due to altered nucleotide sensitivities outweigh their biogenesis and surface expression defects and lead to an overall gain-of-channel-function effect and the neonatal diabetes mellitus disease phenotype (Balamurugan et al., 2019). Here, ABCC8 is linked to neonatal diabetes mellitus.