The acquired AMPK-dependent adult β-cell signature was associated with an increased capacity for glucose-stimulated insulin secretion (GSIS), enhanced β-cell mitochondrial biogenesis, a shift to oxidative metabolism and functional β-cell maturation, whereas in T2DM a remarkable reversion of the normal AMPK-dependent adult β-cell signature to the more neonatal one with increased mTORC1 activation was observed [387]. Here, PRKAA1 is linked to type 2 diabetes mellitus.