reported that DDX5 resolves the G‐quadruplex structure of STAT1 mRNA to promote STAT1 translation and maintain the antiviral effect of IFN‐α in HBV‐related HCC.[42a] In addition, DDX5 induces autophagy and suppresses HCC tumorigenesis by interacting with the autophagic receptor p62, which is independent of its RNA‐binding and helicase activity.[31] Here, we found that the U‐box domain of PRP19 interacts with DDX5 and promotes DDX5 protein degradation by the ubiquitin‐proteasome system in HCC. This evidence concerns the gene STAT1 and hepatocellular carcinoma.