Hepatocytes, activated HSCs, endothelial cells, and immunocytes are involved in the regression of hepatic fibrosis.[74] One possible mechanism is that activated HSCs spontaneously initiate apoptosis or escape apoptosis and revert to an inactive phenotype.[188] Depletion of activated HSCs leads to regression of hepatic fibrosis in several experimental models.[189] Approximately half of activated HSCs or myofibroblasts die after the cessation of CCL4‐induced hepatic fibrosis,[190, 191] during which senescent HSCs inhibit BCL2 expression and ECM production. This evidence concerns the gene CCL4 and Hepatic fibrosis.