Elevated expression of BCL-2 or MCL-1 had no significant impact on the kinetics of morbidity of MLL-AF9-driven AML (Fig. 1d), in contrast to Myc-driven B lymphoid malignancy, which was markedly accelerated by BCL-2 or Mcl-1 transgenes [21, 39]. This evidence concerns the gene KMT2A and acute myeloid leukemia.