Double-strand breaks, both intentional and unintentional, regularly occur in cells. Unintentional breaks are commonly generated by ionizing radiation, various exogenous and endogenous chemical agents, and halted replication forks. Intentional breaks are generated as intermediaries in meiosis and V(D)J recombination, which are primarily repaired through homologous recombination and non-homologous end joining. Both cases require the ends in double strand breaks be processed by nucleases before repair can take place. One such nuclease is Mre11 complexed with Rad50. Mutations of Mre11 can precipitate ataxia-telangiectasia-like disorder.