In other disease models including idiopathic pulmonary fibrosis and liver cirrhosis, LOXL1 was shown to be stimulated by pro-fibrotic TGFB to increase cross-linking, and its knockdown protects from fibrosis and reduces expression of pro-fibrotic metalloproteases and collagens (27). This evidence concerns the gene TGFB1 and pulmonary fibrosis.