Recent studies show that m6A and its RMPs play a critical role in Type 2 Diabetes (T2D) pathogenesis, and ablation of m6A levels by targeting METTL3 or METTL14 in mouse models recapitulates human T2D by inhibiting the Insulin/IGF1-AKT-PDX1 pathway in pancreatic β-cells, resulting in cell-cycle arrest and impaired glucose-stimulated insulin secretion (GSIS) [297]. The gene discussed is INS; the disease is type 2 diabetes mellitus.