Instead, GEMMs have allowed for the investigation of spontaneous ccRCC development and patient therapies within an immunocompetent setting, but the simultaneous mutations involving Vhl with Pbrm1 or Bap1 in these models or the lack of dependence on HIF‐2 for tumorigenesis do not represent the typical developmental timeline of ccRCC [13, 14, 21, 25]. This evidence concerns the gene PBRM1 and nonpapillary renal cell carcinoma.