Literature findings regarding these main targets support YGJD attenuated or even reversed the progression of liver fibrosis among CHB patients by inhibiting fibrosis-related HSC activation and proliferation via RELA, EGFR, OCRL, INPP5B, and HGS, preventing excessive ECM deposition via FN1, JUN, FOS, and MAPK12, and regulating inflammatory response to HBV by regulating both IL-1B and IFNA1. This evidence concerns the gene FOS and Hepatic fibrosis.