Recent studies in a human-derived induced pluripotent stem cell (iPSC) model of neonatal diabetes with a C96R mutation, and in the Akita mouse model of diabetes, in which one Ins2 allele carries a C96Y replacement, suggest that proinsulin misfolding reduces beta cell proliferation and mass due to downregulation of mTOR signalling during pancreas development [55–57], rather than beta cell apoptosis, as it is commonly assumed. Here, INS is linked to diabetes mellitus.