Collectively, these results show that ccRCC cells are sensitive to ATO and suggest that the tumor-inhibitory effects of this compound can be exerted at least in part via pharmacological targeting of PML in p53 proficient cells as well as reactivation of p53 mutants, thus setting the basis for ATO repurposing in ccRCC. This evidence concerns the gene PML and nonpapillary renal cell carcinoma.