RAD51 and glioblastoma: Finally, and more importantly, the results reported here point the way toward a potential therapeutic target that could be exploited to increase the sensitivity of GBM to radiation, a concept that already has support in in vitro studies of inhibition of the c-MET receptor tyrosine kinase, which in turn leads to a decrease in Rad51 expression levels, thereby increasing the radio-sensitivity of GBM cell lines [35].