illustrated that FTO was significantly up‐regulated in certain sub‐types of AMLs such as MLL‐rearranged AML and acute promyelocytic leukaemia.61 Notable enrichment of FTO directly up‐regulated by the oncogenic proteins (e.g. MLL‐fusion proteins, PML‐RARA, FLT3‐ITD and NPM1 mutant) was observed in CD34+ bone marrow cells separated from primary MLL‐rearranged AML patients. The gene discussed is NPM1; the disease is acute myeloid leukemia.