Strikingly, these compounds exert a significantly stronger suppression of proliferation in leukemic cells from AML patients compared to normal myeloid progenitors, underscoring the MYB addiction of AML cells and highlighting the relevance of C/EBPβ as a MYB-p300 cooperation partner for the maintenance of AML cells [84,85]. This evidence concerns the gene MYB and acute myeloid leukemia.