As the first METTL3 inhibitor, 25 has been validated to increase cell differentiation and apoptosis by reducing m6A enrichment in METTL3-dependent core leukemogenic m6A substrates, such as HOXA10 and MYC. As a result, 25 exerts a potent therapeutic effect on multiple AML mouse models by affecting the AML stem cell or leukemia propagating compartment [9]. The gene discussed is MYC; the disease is acute myeloid leukemia.