It has been reported that c-MYC is significantly upregulated in ccRCC and can directly regulate the expression of glucose metabolism genes or induce glycoly-related metabolic enzymes to increase glucose input and synthesis, such as GLUTs, HK2, phosphoglucose isomerase, phosphofructose kinase, glyceraldehyde-3-phosphate dehydrogenase, phosphoglycerate kinase and enolase 45. This evidence concerns the gene HK2 and nonpapillary renal cell carcinoma.