The major role in lung fibrosis is played by M2-type macrophages, which can promote fibrosis through a variety of mechanisms, including the production of TGF-β, CCL18, CHI3L1, MMP, and activation of the Wnt/β-catenin pathway leading to fibroblast activation, myofibroblast differentiation, and ECM remodeling (Shenderov et al., 2021). This evidence concerns the gene TGFB1 and pulmonary fibrosis.