Proteomic analysis of activated HSCs identified STAT1 as a crucial regulator in the transition between liver fibrosis and recovery.86 STAT1 attenuated liver fibrosis by inhibiting HSCs proliferation, reducing TGF-β signaling, and enhancing natural killer cell-mediated killing of activated HSCs.87 In the carbon tetrachloride (CCL4)-induced hepatic fibrosis mouse model, STAT1 knockout mice exhibited significantly faster disease progression compared to the control group.87 Next to STAT1, also STAT3 is playing a crucial role in liver fibrosis. The gene discussed is STAT3; the disease is Hepatic fibrosis.