It has long been purported that the effect of AAT is pleiotropic with strong anti-inflammatory properties, and we can speculate that a genetic predisposition resulting in enhancing the enzymatic degradation of normal host tissue could contribute, in a special environment, to the arthritic phenotype. While most patients with AAT deficiency (AATD) have presented with emphysema or liver disease, it is recognized that the clinical spectrum of AAT diseases is much larger ranging from asymptomatic to severe systemic disease. The gene discussed is SERPINA1; the disease is alpha 1-antitrypsin deficiency.