Upon VSV infection, the overexpression of IRF3-nirs3 downregulates the activity of IRF3 and competes with IRF3 to bind to the IFN-β promoter sequence, thereby significantly inhibiting the IFN-β response and making hepatocellular carcinoma (HCC) more susceptive to viral infection (39). Here, IRF3 is linked to hepatocellular carcinoma.