These results suggested that in the process of liver fibrosis, the permeability of lymphatic vessels was not simply increased by downregulating the expression of Prox1, ZO-1, Esam, etc., but also by upregulating the expression of Claudin-3, etc., to increase the cell junction assembly of hepatic LyECs, implying that the stability of hepatic LVs might reach a balance in positive and negative regulation of tight junction proteins. The gene discussed is CLDN3; the disease is Hepatic fibrosis.