DNA repair has an impact on radiotherapy at two levels. 1: The prolongation of treatment, either by fractionation or decreasing dose-rate allows a greater time for repair during the treatment period resulting in a reduced cytotoxicity in both tumour and normal tissues. 2: DNA repair is an important determinant of variation in cellular sensitivity. Thus variation in normal tissue damage and tumour response may be determined to a significant degree by DNA repair capacity. There have been significant advances recently in the understanding of the mechanisms and genetics of DNA repair in mammalian cells. This includes the identification of the xrcc5 gene as being part of a DNA dependent protein kinase and its association with V(D)J recombination. Such progress holds out promise for the prediction of radiosensitivity of normal and tumour cells and for the rational modification of the radiation response.