An intriguing study also discovered that in individuals with alpha-1 antitrypsin deficiency (AATD), smoking-induced release of EVs from airway epithelial cells increased the expression of CSF2, IL-8, and alpha-1 antitrypsin(AAT) aggregates (potent neutrophil chelators) in AATD macrophages, promoting lung inflammation and damage [44]. Here, CSF2 is linked to alpha 1-antitrypsin deficiency.