ALDH1A3 and type 2 diabetes mellitus: Loss of FOXO1 activity in mouse β-cells leads to dedifferentiation into progenitor-like and α-like cells with re-expression of NGN3, Oct4, Nanog and ALDH1A3 and loss of Pdx1, MafA and Nkx6.1, establishing FOXO1 as a gatekeeper against β-to-non-β lineage drift, and human T2D islets show similar patterns with reduced FOXO1 and β-cell transcription factors, increased ALDH1A3 and “disallowed” genes such as LDHA and MCT1, and a shift toward hormone-negative or α-like endocrine cells [32,34,35,36].