DNA repair proteins like TP53BP1 serveas markers for DNA double-strand breaks (DSBs), which are crucialfor efficient radiotherapy as they lead to cell death. Yang et al. showed the important role of TP53BP1in a radiosensitivity model system using isogenic HCT116 and SW480colorectal cancer cell lines bearing wild-type or various mutant KRASisoforms. KRAS mutations may result inincreased DNA damage, and upregulation of TP53BP1 was found to beassociated with increased nonhomologous end-joining (NHEJ). The gene discussed is KRAS; the disease is cancer.