It has since become widely accepted that the predisposition to the development of basal, panlobular emphysema, as opposed to the apical centrilobular emphysema characteristic of usual COPD, is consequent to an imbalance between serine proteinases (generally considered to be neutrophil elastase) and impaired control of tissue damage and pulmonary inflammation arising from deficiency of α1-antitrypsin (AAT). This evidence concerns the gene SERPINA1 and pulmonary emphysema.