INS and diabetes mellitus: Given the substantial reduction in the proliferation of β cells in the Neurod1CKO mutant, we hypothesized that the deficiency in Ins1 transcription and thus, reduced insulin production, cannot be compensated by increasing the β-cell mass, as reported for the single Ins1−/− deletion mutant [34], and therefore, contributing to the severe diabetes phenotype of our Neurod1CKO.