Combined, these data point to a novel role of SETD2 that can explain the puzzling observation that ccRCC often evade the p53 cell-cycle checkpoint despite a very low frequency of TP53 mutations (Gurova et al., 2004; Dalgliesh et al., 2010; Sato et al., 2013). This evidence concerns the gene TP53 and nonpapillary renal cell carcinoma.