Therefore, notable augmented intimal TGF-β1 and pSmad-2/3 expression across arterial sizes observed by our group also suggest that the Smad-2/3-dependent TGF-β/signalling pathway could be active in IPF arteries, as previously noted in chronic pulmonary vascular disease [41]. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.