In addition to the epidemiologic evidence, recent investigations into PDS and A1AD revealed increased expression of chronic, pro-inflammatory molecules, including 8-nitroguanine, 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG), cyclooxygenase 2 (COX-2), nuclear factor-κB (NFKB), and inducible nitric oxide synthase (iNOS) [16]. The gene discussed is PTGS2; the disease is alpha 1-antitrypsin deficiency.