radiosensitive human syndromes associated with impairment ofHR, likely because this repair pathway is not active in quiescentcells that represent the majority of normal tissue potentially irra-diated during radiotherapy (Massart et al., 2009). Furthermore, theproteins that are essential for NHEJ (Ku70, Ku80, DNA-PKcs) areso important for cell viability that there is no known radiosensi-tive human syndromes associated with mutations in these proteins.By contrast, there are no viable animal models that mimic geneticsyndromes of clinical interest such as BRCA1, BRCA2, ATM het-erozygous mutations that confer high risk of breast or ovariancancer. Hence, the obvious necessity to quantify and to describethe spectrum of radiation responses disappeared behind a numberof