The translocation t(6;11)(q27;q23), resulting in a KMT2A/AFDN fusion gene, is linked to poor clinical outcomes (Kantarjian, 2016; Winters and Bernt, 2017), thus emphasizing the urgent need for new therapeutic approaches for patients with KMT2A-rearranged AML, which led our efforts of searching for alternatives biomarkers. This evidence concerns the gene KMT2A and acute myeloid leukemia.