CCL5 and neoplasm: These cells can enhance immune responses, thereby promoting tumor regression.[18,52] Experimental evidence has shown that tumor IR may trigger RB-dependent senescence, thus augmenting the immunological surveillance of osteosarcoma by natural killer T cells.[53] In pancreatic tumor models, the combination of IR with PARP inhibitors inhibits DNA repair, thereby exacerbating DNA damage and resulting in the production of inflammatory SASP factors including CCL5, IFN-β, and CXCL9/10/11.