Collateral Damage from Antigen Receptor Gene Diversification

Chromosomal translocations that juxtapose antigen receptor genes and oncogenes are frequently associated with lymphoid malignancies. In this issue, show that activation-induced deaminase (AID), an enzyme involved in antigen receptor gene diversification, generates DNA double-strand breaks (DSBs) in oncogenes, and propose that AID and the recombinase-activating gene (RAG) endonuclease may collaborate to generate off-target DSBs.