Increased CXCL8 secretion in breast cancer has been shown to mediate adaptive resistance to PI3K/mTOR-targeted therapy,25 whereas loss of phosphatase and tensin homolog protects breast cancer cells from CXCL8/CXCR1 inhibition,26 indicating that chemokine signaling may promote survival of cancer cells in response to PI3K-targeted therapy. This evidence concerns the gene CXCR1 and cancer.