DNA double-strand breaks (DSBs) are highly cytotoxic lesions that must be repaired appropriately to prevent the formation of deleterious chromosome rearrangements associated with tumorigenesis.Cells use two major pathways to repair DSBs:homologous recombination (HR) and non-homologous end joining (NHEJ).Repair by HR requires a homologous donor duplex and is considered a high-fidelity process,whereas the homology-independent end joining pathway involves re-ligation of the broken ends and is more error prone.