AKT1 and acute myeloid leukemia: Based on the analysis of m6A epigenetic changes in MSCs identified by RIP-qPCR and MeRIP-qPCR, deletion of METTL3 in AML-MSCs can facilitate increased production of AKT protein through controlling m6A modifications of AKT1-mRNA, leading to excessive MSC adipogenesis and consequently making AML cells resistant to chemotherapy.