GTPBP4 and hepatocellular carcinoma: Zhang et al. (2018) found that hypoxic stress in HCC cells can promote the binding of YAP to HIF-1α in the nucleus, maintain the stability of HIF-1α, and activate pyruvate kinase M2 (PKM2) transcription to accelerate glycolysis. In addition, as upstream targets of PKM2, AKT, CAMKβ, and GTPBP4 can also affect the proliferation and glycolysis of HCC cells by regulating PKM2 (Ye et al., 2019; Sheng et al., 2020; Zhou et al., 2022). Similar to oncogenic molecules, Akt can also promote metabolic reprogramming by increasing GLUTs expression (Hu et al., 2019).