Balanced translocations involving MLL at 11q23, RUNX1 at 21q22, CBFB at 16q22, or PML (15q24) and RARA (17q12) are common in this subgroup, suggesting that these cytogenetic subsets of t-MN arise in a lineage committed progenitor cell.3–5 Survival times of t-MN patients are often short, because this disorder is less responsive to current forms of therapy than is AML de novo. The gene discussed is RUNX1; the disease is acute myeloid leukemia.