In clinical samples of t(1;19)-positive ALL, the presence of random nucleotides at the fusion point between E2A- and PBX1-derived exons and the tight clustering of breakpoints in the E2A locus suggest that the translocation may be mediated by the recombinase machinery that normally mediates immunoglobulin gene rearrangements [31]. The gene discussed is PBX1; the disease is acute lymphoblastic leukemia.