Increased β-cell mTORC1 activity plays a critical role in the pathogenesis of T2D [56,57,58,59,60], which is normalized by metformin, an activator of AMP-activated protein kinase (AMPK) and inhibitor of the mechanistic target of rapamycin complex 1 (mTORC1) [61,62]. This evidence concerns the gene PRKAA1 and type 2 diabetes mellitus.