Mouse models of human NDM in which KATP-GOF mutations are expressed in β-cells exhibit chronic hypoglycaemia, persistently low [Ca2+], and impaired glucose-dependent insulin secretion,78,79 and the loss of β-cell mass results from a shift away from mature β-cell identity toward insulin-negative cells, rather than apoptotic cell death.80 This evidence concerns the gene INS and neonatal diabetes mellitus.