Poor survival outcomes in AML are associated with adverse-risk chromosomal lesions (complex karyotype, aneuploidy, t(6;9), inv(3), MLL-fusions), mutations involving TP53 or the RNA splicing/chromatin machinery (RUNX1, ASXL1, BCOR, STAG2, EZH2, SRSF2, SF3B1, U2AF1, ZRSR2 or MLLPTD) [1, 23]. This evidence concerns the gene KMT2A and acute myeloid leukemia.