Notably, in the untreated group, the protein expression levels of pro-fibrotic mediators TGF-β, p-Smad2, and p-Smad3 were markedly elevated compared with the healthy group in the CCL4‐induced liver fibrosis model, consistent with the hyperactivation of this pathway during fibrosis progression. The gene discussed is SMAD2; the disease is Hepatic fibrosis.