Gerritsen et al. subdivided AML patients on the basis of two recurrent genetic alterations, the RUNX1 mutation and t(8;21), and observed that, as compared to t(8;21), the RUNX1 mutation is able to initiate a specific transcriptional program that provides an important contribution to leukemic transformation. The gene discussed is RUNX1; the disease is acute myeloid leukemia.