In myofibroblasts, M2 macrophages are activated, leading to increased secretion of TGF-β, which leads to the activation of the TGF-β/smad2 signaling pathway; in mouse models of pulmonary fibrosis, the increase in M2 macrophages was accompanied by the increase in TGF-β1 and p-smad2/3 proteins [20, 21]. Here, SMAD2 is linked to pulmonary fibrosis.