Resistance to radiation is a major challenge in the treatment of Glioblastoma. A subset of tumor cells is capable of modulating their DNA damage repair pathway to escape apoptosis, mechanisms of which are still unknown. Since the physiological substrate of DNA damage repair machinery is packed into chromatin, the efficiency of DNA damage repair in a cell must depend on how well the repair factors can gain access to the damaged DNA. Histone modification and chromatin re-modelling are the most important determinants of DNA accessibility.