DNA double strand breaks arise endogenously in the cell as a result of routine activities such as metabolism and also as a result of exposure to exogenous agents such as ionising radiation. Repair of DNA DSBs is coordinated by two major repair pathways in mammalian cells; non-homologous end joining and homologous recombination. Nonhomologous end joining is the dominant repair pathway during G1 and G2 phase of the mammalian cell cycle. The core non-homologous end joining factors Ku, DNA-PKcs, XLF, DNA Ligase IV and XRCC4 are essential for efficient and accurate rejoining of double strand breaks. In 2004, Riballo et al. discovered that the ATM protein kinase and the Artemis endonuclease were important for repair of a fraction of DNA double strand breaks in G1 phase cells.