Molecularly, Smad4 expression in hepatocytes upregulated the expression of ID1 and further enhanced the paracrine activity of CTGF; subsequently, mediated by EGFR, CTGF promoted HSCs’ activation by regulating the p38 and p65 signaling pathways, which in turn led to liver fibrosis. The gene discussed is ID1; the disease is Hepatic fibrosis.