However, although we see a significant reduction in the organ-specific metastasis of RCC cells in response to CXCL12 depletion, we cannot exclude the possibility that small amounts of non-neutralized CXCL12 remain in the tumor microenvironment and may contribute to angiogenic and proliferative responses within the primary tumor. This evidence concerns the gene CXCL12 and renal cell adenocarcinoma.