27, 34). In both db/db mice and early-stage human T2DM, loss of nuclear MafA represents one of the earliest molecular signatures of dysfunction (8, 35). Furthermore, FoxO1 ablation in adult mouse β-cells has been shown to induce expression of progenitor markers like Ngn3, Oct4, and Nanog, further supporting its role in maintaining β-cell maturity (19, 29, 36–38). Here, MAFA is linked to type 2 diabetes mellitus.