Current research suggests that sEVs are important players in the pathogenic states of bronchial epithelium, such as the development of asthma; sEVs are released from airway epithelium and carry miRNAs (miR-34a, miR-92b, miR-210) that may impact the Th2-dependent immune response in asthma [52], and sEVs derived from mesenchymal stroma cells influence Treg suppression through the activation of peripheral blood mononuclear cells (PBMCs) to secrete IL-10 and TGF-β. This evidence concerns the gene TGFB1 and asthma.