In this study, CKI targeted Smad7 and upregulated its expression to induce TGFβR1 degradation and subsequently inhibited the phosphorylation of Smad2 and Smad3 to suppress TGF‐β/Smad2/3 signaling in activated HSCs, suggesting rebalanced TGF‐β/Smad7 signaling by CKI as a novel strategy in the treatment of liver fibrosis and oncogenesis. The gene discussed is TGFBR1; the disease is Hepatic fibrosis.