Restoration of mTORC1 activity in Akita β-cells increased β-cell expansion and ameliorated diabetes without increasing PDX-1 and NKX6.1 expression and glucose-stimulated insulin secretion, further indicating that β-cell growth arrest induced by mTORC1 inhibition plays a key role in the pathophysiology of permanent postnatal diabetes. This evidence concerns the gene PDX1 and diabetes mellitus.