Recent studies imply that DNA repair should not be simply regarded as an intrinsic property of tumor cells, but a biological process that could be activated by environmental cues.39 Together with previous studies, our results unveil that hyperactivated CCL5-CCR5 signaling governs DNA repair activation in tumors.28 In the context of GBM, pericyte-secreted CCL5 binds to CCR5 expressed on GBM cells triggering the activations of AKT and downstream DNA-PKcs to promote DDR, thus overcoming the TMZ-induced cytotoxicity. This evidence concerns the gene AKT1 and glioblastoma.