The inherently immunogenic nature of ccRCC, characterized by frequent inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene, resulting in aberrant hypoxia-inducible factor 2α (HIF-2α) stabilization, and overproduction of pro-angiogenic factors such as VEGF and platelet-derived growth factor (PDGF), provided a strong biological rationale for immunotherapy [5,6,7]. The gene discussed is VHL; the disease is nonpapillary renal cell carcinoma.