FBP1 and neoplasm: Another research showed that FBP1, which was the crucial enzyme in gluconeogenesis, was general absence in ccRCC.[51] They provided an opinion and relevant evidence that FBP1 worked as an opposer by antagonizing both HIF mediated hypoxia adaption responses and glycolytic flux within tumor tissue in ccRCC progression.[51,52] However, further clinical trials are needed to validate our observations and the mechanisms underlying the prognostic value of these genes in ccRCC also deserve further experimental exploration.