In the present study, we demonstrate a positive regulatory loop between the fusion protein AML1-ETO and FTO, which exerts a critical role in promoting leukemogenesis and resistance of t(8;21) AML cells to Ara-C by modulating the expression of its mRNA targets, such as IGFBP2, via m6A demethylation (see the proposed model in Fig. 8H). The gene discussed is IGFBP2; the disease is acute myeloid leukemia.