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. Here, FBP1 is linked to nonpapillary renal cell carcinoma.