Balanced chromosome rearrangements between 11q23 and other chromosomes, present in ~5% of de novo AML, generate several distinct KMT2A fusion proteins,8 the most frequent of which are MLLT3 (not considered an adverse karyotype), MLLT1, MLLT10, ELL and MLLT4.9 In KMT2Ar-AML, the c-terminal portion of KMT2A – responsible for the methyl transferase activity of the enzyme – is replaced by a region of the fusion partner that leads to the recruitment, probably indirectly in most of the cases, of the DOT1L and TEFb complexes to the KMT2A fusion binding sites. This evidence concerns the gene ELL and acute myeloid leukemia.