We have also demonstrated that the release of profibrotic EVs, mediated by ASK1‐ER stress, plays a key role in the interaction between alveolar epithelial cells and pulmonary fibroblasts during MV‐induced pulmonary fibrosis.[45] Consistently, our present study shows that ITGβ1 transfer, mediated by profibrotic EVs, represents a novel mechanism underlying fibroblast activation and the progression of SAPF. The gene discussed is ITGB1; the disease is pulmonary fibrosis.