These authors also found there are no indications of MDM2, MDM4, or ARF involvement in the functional repression of p53 in RCC; instead, p53-mediated transactivation can be activated by lentivirus vector-driven high-level expression of p53; and p53 inactivation prevailed in the hybrids of RCC cells with the cells possessing fully functional p53 [142]. This evidence concerns the gene TP53 and renal cell carcinoma.