Mechanistically, we show that genetic ablation of Stat3 in murine as well as knockdown of STAT3 in human cells resulted in an increase of nuclear factor-kappa B (NF-κB)-induced expression of the pro-angiogenic chemokine ligand 1 (CXCL1; murine orthologue to the human IL-8), thereby promoting tumour growth. The gene discussed is CXCL8; the disease is neoplasm.