[en] Ionizing radiation (IR) induced DNA double-strand breaks (DSBs) are primarily repaired by non-homologous end joining (NHEJ) while a subset DSBs which are accumulated in G2 phase are repaired by homologous recombination (HR). DNA repair-deficient tumor cells have been shown to accumulate high levels of DNA damage. Consequently, these cells become hyperdependent on DNA damage response pathways, including the CHK1-kinase-mediated HR-repair. These observations suggest that DNA repair-deficient tumors should exhibit increased radio-sensitivity under HR-inhibition. Genetic defects leading to functional loss of Werner (WRN) protein is associated with genomic instability and increased cancer incidence. In the current investigation, using isogenic pairs of cell lines differing only in the WRN-function, we showed that WRN-deficient cell lines were hyper-radiosensitive to CHK1 pharmacologic inhibition