In AML, writers (such as METTL3, METTL14, and METTL16), erasers (FTO and ALKBH5), and readers (YTHDF1, YTHDF2, YTHDC1, and IGF2BP2) are all aberrantly upregulated, promoting AML progression.4, 28. This evidence concerns the gene YTHDF2 and acute myeloid leukemia.