In addition, Zhang et al. discovered the key potential transcription axis of CTCF/POLR2A—SYNJ2/INPP5B in metabolic programs based on the ChIP-seq data set, speculated that CTCF/POLR2A could directly dysregulate SYNJ2 levels and that increased SYNJ2 would affect HCC development via metabolic perturbation pathways (Zhang et al., 2021). This evidence concerns the gene SYNJ2 and hepatocellular carcinoma.