These genes included cytokines and effector molecules suggestive of a broad immune activation, but interestingly, the sole exception was the expression of PRF1. Bearing in mind the overall high T cell infiltration of ccRCC [39,62] and the negative prognostic impact of IFNγ, we propose here that an “unfavorable” T cell inflammation with high levels of IFNγ and low PRF1 expression might be driven by RCC lipid metabolism. This evidence concerns the gene PRF1 and nonpapillary renal cell carcinoma.