While fibroblasts with α-SMA expression did not contribute significantly to the lung fibrosis induced by bleomycin or the kidney fibrosis induced by unilateral ureter obstruction, they did contribute significantly to the liver fibrosis induced by CCl4, as the deletion of αv integrin in α-SMA-expressing cells protected against the experimental fibrosis in the liver but not in the lung or kidney [35]. This evidence concerns the gene ACTA1 and Hepatic fibrosis.