However, by quantifying the thickness of extracellular matrix and cell number of macrophages (F4/80+) and neutrophils (Ly6G+) around small airways (Figure S11, Supporting Information), we found that COPD‐specific bronchitis phenotypes generally induced by cigarette smoke did not arise in our elastase‐induced emphysema model, and EV administration did not induce and alter small airway inflammation and fibrosis.[27] Only 0.2% of cells were positive for Sftpc and Ki67, markers of proliferating AT2 cells, in the lungs of mice receiving elastase instillation. This evidence concerns the gene MKI67 and bronchial disorder.