Consequently, excessive myoblast proliferation ensues, instigating IPF development (85–87); secondly, PDL1 mediates the transition of pulmonary fibroblasts into myofibroblasts and instigates EMT induction via TGF- β, facilitated by the Smad3 and β-catenin signaling pathways, thereby promoting fibrosis (88, 89); thirdly, upregulation of PDL1 in pulmonary fibroblasts hampers autophagy-induced myofibroblast proliferation and ECM deposition, ultimately leading to pulmonary fibrosis. Here, CD274 is linked to idiopathic pulmonary fibrosis.