In keeping, breast cancer CSC were shown to proliferate in vitro in response to the addition of exogenous CXCL8 while a small molecular weight antagonist of CXCR1/2 (reparixin) (8) or a blocking anti-CXCR1 (but not anti-CXCR2) monoclonal antibody were both able to deplete CSC in vitro (9). This evidence concerns the gene CXCR1 and breast carcinoma.