MYB and acute myeloid leukemia: Recent genome-wide studies have demonstrated that Myb, C/EBPβ and p300 together with several other hematopoietic transcription factors and the bromo-domain protein BRD4 co-localize at many genomic sites in AML cells to stimulate the activity of so-called “super-enhancers” that are involved in maintaining the proliferation of the leukemic cells [11].