CircRPN2 accelerated ENO1 degradation and promoted glycolytic reprogramming through the AKT/mTOR pathway, thereby inhibiting HCC aerobic glycolysis and metastasis (35); plasma exosomal circLPAR1 specifically bound to eIF3h and inhibited the METTL3-eIF3h interaction, which reduced the translation of the oncogene BRD4 and inhibited CRC growth (36). This evidence concerns the gene EIF3H and hepatocellular carcinoma.