For pulmonary diseases, Willis et al. [47] reported both in vivo and in vitro that UCMSC-EXOs effectively regulate macrophage phenotypes, suppressing proinflammatory M1 states (CCL2, CCL7, and IL-6) while promoting anti-inflammatory M2-like states (arginase-1, CD206, and CCL17), and these findings demonstrate the potential of UCMSC-EXOs to alleviate bronchopulmonary dysplasia induced by hyperoxia by normalizing lung function, reducing fibrosis and pulmonary vascular remodeling, and ameliorating pulmonary hypertension. This evidence concerns the gene CCL17 and lung disorder.