The avoidance of pFAK activation by CXCR1/2 inhibition in breast cancer cells results in sensitization and reduction of migrative potential of stem cells, while the inhibition of the same pathway in peripheral sensory neurons, promoted by taxane treatment via exocrine and endocrine IL-8 production, may efficiently prevent microtubule acetylation, terminal axons arborization and synaptic plasticity thus modulating the key features of chemotherapy-associated neurotoxicity. This evidence concerns the gene CXCR1 and breast cancer.