In sum, our results suggest that, unlike the senescence process that is induced by PML depletion in TNBC, which is p53-independent (Arreal et al, 2020), suppressing PML expression in ccRCC provokes a phenotype of growth arrest that is mediated by p53 and its target gene network. The gene discussed is TP53; the disease is nonpapillary renal cell carcinoma.