Pulmonary fibrosis (PF) from cigarette smoke is partly due to subsequent enrichment of HBE exosomes with miR-21, which, when taken up by fibroblasts, modulates the TGF-β1/Smad3 pathway to increase collagen and α-SMA expression (Fig. 3A) [71]. The gene discussed is SMAD3; the disease is pemphigus foliaceus.