Recent work has demonstrated co-localization of C/EBPβ, MYB, and p300 at multiple genomic sites in AML cells [28], implying that these factors also co-operate in AML and thus providing a conceptual framework for how C/EBPβ can contribute to the pro-leukemogenic function of MYB. The gene discussed is CEBPB; the disease is acute myeloid leukemia.