This hypothesis is further supported by our observation that levels of the hypoxia-induced chemokine CXCL12 and its receptor CXCR4, which have been involved in tumor vascularization, invasion and lack of sunitinib efficacy [25, 43, 44], were increased in tumors that progressed, but not significantly altered in our in vitro experiments using sunitinib-resistant RCC cell lines. This evidence concerns the gene CXCL12 and neoplasm.