Further, our data demonstrated that blockage of autophagic flux reversed EGCG-mediated inhibition of HMGB1 release, NLRP3 inflammasome activation and the subsequent liver fibrosis progression in rcccDNA mice, supporting the autophagic degradation of HMGB1 as a key mechanism for EGCG’s therapeutic effect on HBV-induced liver fibrosis. The gene discussed is NLRP3; the disease is Hepatic fibrosis.