Macrophages play a dual and dynamic role in the pathogenesis of idiopathic pulmonary fibrosis (IPF), shifting from a proinflammatory M1 phenotype in the early stages—characterized by cytokine release, oxidative stress, and ECM remodeling—to a profibrotic M2 phenotype in advanced disease, marked by the secretion of TGF-β, PDGF, and other mediators that drive fibroblast activation and collagen deposition [99]. Here, TGFB1 is linked to pulmonary fibrosis.