Compared to CCl4 group, CKI inhibited abnormal cell proliferation of HCC tumors and surrounding normal liver tissues (Figure 8H), suggesting CKI exerted a similar underlying mechanism between attenuating chronic liver fibrosis and inhibiting HCC formation by upregulating Smad7 expression to inhibit TGF‐β/Smad signaling. Here, TGFB1 is linked to hepatocellular carcinoma.