Model for susceptibility to chromosome translocations mediated by V(D)J recombinase. Antigen receptor diversification is initiated by DNA breaks, mediated in the case of V(D)J recombination by the Rag-1 and Rag-2 proteins at RSS-coding segment borders (depicted by triangles and squares, respectively). The normal rejoining process resolves both sets of DNA ends efficiently, so that the potential for aberrant recombination is minimal. Failure of the normal rejoining process triggers cellular DNA damage sensors, which effect cell death and thereby prevent oncogenic rearrangements. Impairment in cellular DNA damage responses may allow alternative DNA repair pathways to mediate rejoining of antigen receptor genes with sites elsewhere in the genome—sometimes including oncogene loci, which give rise to lymphoma-associated chromosome translocations.