Abnormal A1AT activity or deficiency is associated with COPD emphysema. However, it should be noted that environmental exposures, such as cigarette smoke or poor air quality, are more pertinent risk factors than genetics. A1AT's protective effects primarily arise from its role in neutrophil regulation. A1AT enters the lungs via passive diffusion and are taken up by pulmonary epithelial cells via clathrin‐dependent endocytosis. This process irreversibly inhibits neutrophil elastase (NE). It functions as a neutrophil chemotaxis modulator by binding to IL-8 which prevents it from interacting with CXCR1. Additionaly, A1AT inhibits ADAM17 which prompts cell migration during inflammation.