Paris et al. (2019) pointed out that YTHDF2 was not essential for normal HSC function; however, increased expression of YTHDF2 was required for both initiation and propagation of AML, contributing to the integrity of LSC function by decreasing stabilities of m6A transcripts including the tumor necrosis factor receptor Tnfrsf2. Importantly, the upregulation of Tnfrsf2 in Ythdf2-deficient LSCs primed malignant cells for apoptosis, predicting YTHDF2 as a potential therapeutic target in patients with AML to selectively inhibit LSCs and promote the expansion of HSCs (Paris et al., 2019). This evidence concerns the gene YTHDF2 and acute myeloid leukemia.