Although this is not a functional proof, the significant enrichment of RUNX1 heptamer motifs at the deletion borders in conjunction with our Runx1−/− mouse TCRβ data clearly argues for an involvement of RUNX1 not only in physiological deletions but also for a major role for the generation of pathological deletions in ETV6-RUNX1 ALL. The gene discussed is RUNX1; the disease is acute lymphoblastic leukemia.