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. The gene discussed is METTL14; the disease is acute myeloid leukemia.