IL8 signal, via two cell surface G-protein–coupled receptors CXCR1 and CXCR2, has been shown to be upregulated in several types of cancer including breast cancer and associated with increased CSC pool in vitro and poor prognosis in patients.33, 34, 35 Our in vitro data demonstrated that blockade of IL8 with a neutralizing antibody or blockade of IL8 receptors CXCR1 and CXCR2 with reparixin inhibits autocrine inflammatory forward-feedback loop triggered by paclitaxel treatment (Figures 4 and 5). This evidence concerns the gene CXCR2 and breast carcinoma.