It is known that in non-AATD COPD, efferocytosis by alveolar macrophages is reduced,56 and since the inflammatory and neutrophilic response in AATD is enhanced this is likely to be a pathologically important pathway.24 Further, supplementation of macrophages in vitro with exogenous AAT restores cigarette smoke induced decrease in efferocytosis, suggesting AAT is protective to macrophages, although the mechanism is currently unknown.48 This evidence concerns the gene SERPINA1 and alpha 1-antitrypsin deficiency.