Most importantly, the addition of CCL5 neutralizing antibody significantly boosted the tumor-suppression role of PARPis in both BRCA1/2-wild type and BRCA1/2-mutant xenografts (Fig. 5e, f and Supplementary Fig. 4d, e), accompanied with partial reversal of PARPi-induced stromal activation (Fig. 5g and Supplementary Fig. 4f-h), indicating that this enhanced tumor growth inhibition may be partially due to the elimination of CCL5 exertion on sustaining stromal fibroblast activation. Here, BRCA1 is linked to neoplasm.