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. Here, EP300 is linked to acute myeloid leukemia.