In HGSOC cells SKOV3, CXCR2 KD comprised secretive activity of CXCL1 and CXCL8 [24] and, likewise our results, led to decreased cell viability, suggesting that silencing CXCR2 expression suppressed OC tumorigenicity in vivo and in vitro. Metastatic breast cancer cells can be re-sensitized to paclitaxel and doxorubicin by CXCR2 KD [41], as CXCR2 blockade was correlated to increased overall therapeutic response to antineoplastic substances, possibly due to lower TG and metastasis indexes [33, 41]. This evidence concerns the gene CXCL1 and breast carcinoma.