CXCR1 and neoplasm: In search of the mechanism(s) involved in the sensitization of HNSCC tumor cells to docetaxel, we found that blockade of CXCR1/2 increased the expression of miR-200c, a pleiotropic tumor suppressor known to inhibit tumor growth, increase susceptibility to chemotherapy, and block EMT through its main target, ZEB1 [40].