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]. The gene discussed is VHL; the disease is nonpapillary renal cell carcinoma.