For example, Liang et al. considered CAV1 as an oncogene in bladder cancer as it promotes invasive phenotypes by inducing EMT through Slug overexpression, and the whole process occurs through the activation of PI3K/AKT signaling pathway [24] and Henriett Butz et al. found that CAV1 protein was upregulated in ccRCC compared to its normal counterparts and it was associated to patient survival [25]. This evidence concerns the gene SNAI2 and nonpapillary renal cell carcinoma.