These findings appear consistent with a spectrum in the molecular pathogenesis of early-onset and late-onset diabetes caused by autosomal dominant INS gene mutations, ranging all the way to proinsulin-G(C28)R [7] which ultimately generates perfect human insulin lacking any mutation, does not use the MIDY mechanism (this report) and instead operates either through novel mechanisms involving the mutant C-peptide [15] or is coincidental to the pathogenesis of diabetes. Here, INS is linked to Onset.