PRDX3 silencing exacerbates liver fibrosis and HSC activation, while HSC overexpression of PRDX3 alleviates liver fibrosis caused by CCl4 by inhibiting HSC activation through the mitochondrial ROS/TGF-β1/Smad2/3 signalling pathway [37]. This evidence concerns the gene SMAD2 and Hepatic fibrosis.