Conversely, in both AML types, the reduction of C/EBPα-binding activity by either knockdown (Ptasinska et al., 2014) or expression of a dominant-negative version of C/EBP (DNCEBP) blocks myelopoiesis and abolishes the upregulation of genes required for terminal myeloid function (MPO, CSF1R, and CTSG). The gene discussed is CSF1R; the disease is acute myeloid leukemia.