Among many genetic factors that were found to be related to ccRCC, the inactivation of Von Hippel–Lindau (VHL) tumor suppressor gene occurs in 80% of patients and is the most common event (7–9), leading to the interruption of both vascular endothelial growth factor (VEGF) and mammalian target of rapamycin (mTOR) signaling pathways, which serve as the targets of most of the drugs currently used in clinical practice (10, 11). The gene discussed is VHL; the disease is nonpapillary renal cell carcinoma.