Their results suggest that the chemokine CXCL5 (produced by bone cells) and its receptor CXCR2 (expressed on breast cancer cells) are major signaling mediators that govern the rate of CTC extravasation and the extent of migration, indicating the possibility of CXCL5-CXCR2 inhibition as a therapeutic target. This evidence concerns the gene CXCR2 and breast cancer.