Overall, this argues strongly for an intimate and more general role of C/EBPβ, together with the co-activator p300, in supporting the oncogenic potential of MYB in AML, and leads to a model in which MYB, C/EBPβ and p300 cooperate in a transcriptional module to control the expression of genes that are critical for maintaining the viability of AML cells and preventing their differentiation. This evidence concerns the gene CEBPB and acute myeloid leukemia.