Studies have demonstrated that downregulation of METTL3 in acute myeloid leukemia (AML) cells resulted in cell cycle arrest, differentiation, apoptosis, and delays in leukemia progression in vivo.2,3 Furthermore, the loss of METTL3 and m6A induces aberrant dsRNA formation in hematopoietic cells, triggering an innate immune response and cell death.4 Pharmaceutical inhibitor STM2457, targeting METTL3, has shown remarkable effectiveness in reducing AML growth in vitro and in vivo,5 emphasizing enzymatic inhibition of METTL3 as a promising strategy for anticancer therapy. Here, METTL3 is linked to acute myeloid leukemia.