The most critical antiprotease deficiency triggering COPD is that of α-1-antitrypsin (AAT), which plays a vital role in neutrophil elastase inhibition and other proteases such as proteinase-3, cathepsin G, caspase-3, and neutrophils serine protease-4 [206,207,208]. This evidence concerns the gene PRTN3 and chronic obstructive pulmonary disease.