Although p300 acts as a co-activator for many transcription factors [66], we presume that the addiction of AML cells to high levels of MYB activity as well as the synergistic interplay of MYB and C/EBPβ and their simultaneous inhibition via p300 may explain why the compound preferentially inhibits AML cells versus normal hematopoietic progenitor cells or non-hematopoietic cells. This evidence concerns the gene CEBPB and acute myeloid leukemia.