Consistent with the murine OB providing a radioresistant niche for GBM cells [6], the γH2AX and 53BP1 foci analyses presented here show that, while initial levels of radiation-induced DSBs are similar, tumor cells in the OB have an increased capacity to repair the DNA damage as compared to those in the RH. This evidence concerns the gene TP53BP1 and glioblastoma.