For example, in acute myeloid leukemia patients with the chromosomal translocation t(8; 21), the abnormal AML1-ETO fusion protein appears to misdirect HDAC1 containing corepressor complexes to AML1 binding sites, repressing genes needed for myeloid differentiation and resulting in leukemogenesis9–11. The gene discussed is RUNX1; the disease is acute myeloid leukemia.