Endogenous and exogenous production of H2S in the liver and its effects on liver fibrosis. H2S plays a complex role in the development of fibrosis. Besides as a reducer to directly scavenge reactive oxygen species, exogeneous (NAHS, GYY4137) or endogenous H2S utilizes its inhibitory effect on fibrosis by anti-inflammation and suppression of fibroblasts activation. Many signaling pathways, such as TNF-α, NF-κB, MAPKs, NRF2, SIRT1, SIRT3, GSH, TGF-β1/SMAD, PI3K, AKT, and autophagy are involved in the process of antifibrosis of H2S. TNF-α: tumor necrosis factor-alpha; NF-κB: nuclear factor-kappa B; MAPK: mitogen-activated protein kinase; NRF2: nuclear factor erythroid 2–related factor 2; SIRT1: sirtuin 1; SIRT3: sirtuin 3; GSH: glutathione; TGF-β1: transforming growth factor beta 1; SMAD: suppressor of mothers against decapentaplegic; PI3K: phosphoinositide 3-kinase.