Further gain- and loss-of-function experiments evidenced that overexpression of CXCR4 promoted cell proliferation, viability, migration, epithelial-mesenchymal transition (EMT) and tumor formation in vitro and in vivo, while knock-down of CXCR4 had opposite effects on the above cellular functions and induced ccRCC cell apoptosis, implying that CXCR4 promoted RCC progression, which were supported by the previous literatures in other types of cancer [39–42]. The gene discussed is CXCR4; the disease is neoplasm.