A recent study presented by Sheng’s group [108] found that YTHDC1, a nuclear m6A reader, is highly expressed in AML and that it contributes to the maintenance of AML cell proliferation and progression; knockdown of the YTHDC1 gene significantly blocked the proliferation of primary AML cells via modulating MCM complex-mediated DNA replication, as well as the self-renewal of LSCs in vivo in mice, thus achieving control of leukemogenesis. This evidence concerns the gene YTHDC1 and acute myeloid leukemia.