Until 2019, Paris et al. [20] declared that YTHDF2 was overexpressed in human AML and the up-regulation of YTHDF2 played an important role in the development of LSC and the initiation and propagation of AML partly through shortening the half-life of multiple m6A transcripts which were closely related with LSC function. This evidence concerns the gene YTHDF2 and acute myeloid leukemia.