Such inducible features of FTO-mediated m6A hypomethylation are further strengthened by the fact that TKI-resistant primary clones possess a more robust FTO-m6A pathway compared to parental clones, even when their clone sizes are similar, and that nilotinib therapy in AML patients increases FTO expression but deceases m6A methylation. This evidence concerns the gene FTO and acute myeloid leukemia.