Thus, ATRA treatment was able to (i) reduce the expression of collagen types I, III, and IV, fibronectin, laminin, elastin, and proteoglycans; (ii) downregulate the expression of TGF-β1, CTGF, and TGF-β receptor 2; (iii) suppress TGF-β1-induced Smad2/3 phosphorylation; and (iv) increase the expression of MMPs, such as MMP-2 and MMP-3, in various fibrosis models [39,40,41,42,43,44]. The gene discussed is ELN; the disease is fibrosis.