Genomic loss of the Von Hippel-Lindau (VHL) tumour suppressor, arginase 2, argininosuccinate synthetase (enzymes involved in the urea cycle), the progression of arginine, glutamine, tryptophan, glutathione, cysteine/methionine metabolism, polyamine, and activation of HIF2a-mediated pro-oncogenic signalling are the most well-known metabolic disturbances in ccRCC [1,3,7]. The gene discussed is VHL; the disease is nonpapillary renal cell carcinoma.