We first reported that FTO is highly expressed in acute myeloid leukemia (AML) with t(11q23)/MLL-rearrangements, t(15;17)/PML-RARA, FLT3-ITD and/or NPM1 mutations, and enhances leukemic malignant transformation and leukemogenesis as an m6A demethylase.3 Subsequently, we showed that R-2-hydroxyglutarate (R-2HG), an oncometabolite of mutant isocitrate dehydrogenase 1/2 (IDH1/2), exerts a broad and intrinsic antileukemic activity through competitively inhibiting the demethylase activity of FTO.1 Such identification indicates that FTO might act as a druggable target for leukemia therapy. Here, KMT2A is linked to acute myeloid leukemia.