METTL3 and type 2 diabetes mellitus: Depletion of METTL3/14 in endocrine progenitors implicated that METTL3/14 were dispensable for beta-cell differentiation but modulated expression of an essential transcription factor MAFA, leading to hypo-insulinemia and hyperglycemia.198 The m6A reader IGF2BP2 is identified as crucial for β-cell proliferation, PDX1 expression level, insulin secretion, and further related with T2DM susceptibility.