The report indicated that the higher renal venous levels may be a consequence of alterations in the hypoxia-induced pathway in renal cancer, associated with the loss of von Hippel–Lindau (VHL); accumulation of hypoxia-inducible factor (HIF)-1α; and consequent overexpression of VEGF, PDGF-AB/BB, and TGF-β1, which are then upregulated in renal venous blood [83]. This evidence concerns the gene VEGFA and renal carcinoma.