We hypothesized that targeting thyroid cancer cells using the selective CXCR2 receptor antagonist AZD5069 may reduce the CXCL8-mediated pro-tumorigenic effects (i.e. via inhibition of cell migration) and/or suppress the tumour cell ability to secrete CXCL8 endogenously. This evidence concerns the gene CXCL8 and neoplasm.