It is reported that in clear cell renal cell carcinoma, high expression of SLC2A5 increased tumour cells growth, while the deletion of SLC2A5 dramatically attenuated cellular malignancy via activating the apoptotic pathway.38 Some articles claimed that SLC2A5-mediated fructose utilisation drove lung cancer growth by stimulating fatty acid synthesis and AMPK/mTORC1 signaling.39 Therefore, it seemed that the studies involving the mechanism of SLC2A5 were still limited to the downstream level of the molecule. This evidence concerns the gene SLC2A5 and neoplasm.