However, the anticancer effects of STAT3 and NF-κB inhibitors are limited, and these drugs may produce several side effects after long-term treatment [50, 51]; therefore, the usage of anti-CCL-16 antibodies to block the interaction of CCL-16 with its receptors may become an attractive strategy to block the interaction between CCL-16 and its receptors in treating hepatitis, preventing liver inflammation and HCC development. Here, STAT3 is linked to hepatitis A virus infection.