The origin of this theory was the observation that patients with α1-antitrypsin (an anti-protease) deficiency (AATD) develop early onset emphysema [17] implicating a role for its target enzymes (neutrophil elastase and proteinase 3), which can induce many of the features of COPD in animal models[18]. The gene discussed is PRTN3; the disease is chronic obstructive pulmonary disease.