Together, these publications indicated that ELR+ CXC chemokines—derived from autocrine or paracrine sources—induced signaling through CXCR1/CXCR2, leading to increased tumor cell proliferation, viability and anchorage independent cell growth; the chemokines also reduced the levels of tumor cell apoptosis, and inhibition of these chemokine pathways caused cell cycle arrest. The gene discussed is CXCR2; the disease is neoplasm.