Members of the CBF complex are commonly perturbed during leukemogenesis and are frequent targets of translocation in T cell acute lymphoblastic leukemia (T-ALL), myelodysplastic syndromes (MDS), acute myeloid leukemia (AML), and B-cell acute lymphoblastic leukemia (B-ALL)5,6,7 Missense mutations within the DNA binding domain of RUNX1 are recurrent events in T-ALL (10–15% cases) suggesting a tumor suppressor role.8 Here, CEBPZ is linked to myelodysplastic syndrome.