The anti-protease alpha-1-antichymotrypsin (SERPINA3) manipulates the immune and inflammatory response through inhibition of chymotrypsin and cathepsin G. Previous studies have identified increased SERPINA3 in serum from COPD subtypes associated with metabolic syndrome [26], with genetic mutations resulting in SERPINA3 deficiency resulting in milder disease in patients with COPD [27] and cystic fibrosis(CF) [28]. This evidence concerns the gene CTSG and metabolic syndrome.