The study of the mechanism indicated that altered intestinal permeability presented as down-regulation of tight junction proteins (occluding, claudin-1) in colitis mice may favor the passage of bacterial products such bacterial LPS into the liver through the portal vein, and then increased LPS activated TLR4 signaling and HSCs activation which involved in liver inflammation and fibrogenesis (Figure 6). The gene discussed is CLDN1; the disease is colitis.