A number of potential mechanisms underlying varying responses have been proposed with preclinical studies demonstrating an up-regulation of the production of the pro-angiogenic cytokine IL-8 associated with the development of sunitinib resistance, the same study found that the tumours in murine models were subsequently re-sensitised to sunitinib following the administration of an IL-8 neutralising antibody and began to respond to therapy despite previous failure [50]. This evidence concerns the gene CXCL8 and neoplasm.