We favor this explanation for the reasons that (1) genes encoding key nodes of the IFN system, including IFN-β and IRF-7, contain functional NF-κB sites in their promoters [53,54], and simple activation of NF-κB can drive these promoters [43,54]; (2) a 1:1 correlation was found between ccRCC samples that contained nuclear NF-κB and those that displayed activated STAT1, and (3) the IFN signature collapses in cells lacking the NF-κB subunit RelA (Figure 7a). This evidence concerns the gene IFNB1 and nonpapillary renal cell carcinoma.