As the elastolytic ability of PR3 is less than NE, PR3 likely plays a lesser role in the manifestation of emphysema.71 In contrast, however, anti-PR3 autoantibodies have been proposed to exacerbate the degranulation process by binding PR3 expressed on surface membranes of monocytes and neutrophils, resulting in excess protease release and contributing to both vascular and endothelial injuries.71,72. The gene discussed is PRTN3; the disease is pulmonary emphysema.