In addition, GLI1 overexpression by normal kidney tubular cells showed enhanced tumorigenic abilities with tumor-formation rates in an animal model [42], and the GLI1 expression level was significantly correlated with OCT4 and Nanog levels in ccRCC specimens, suggesting that GLI1 plays a critical role in the initiation and progression of ccRCC via upregulating OCT4 and Nanog. This evidence concerns the gene POU5F1 and nonpapillary renal cell carcinoma.