It is well known that IL-32 plays significant pathophysiological roles in the development of several inflammatory diseases, such as arthritis, psoriasis, ulcerative colitis, Crohn’s disease, and chronic obstructive pulmonary disease [3–6], since it alters the release of pro and anti-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), IL-1β, IL-6, and IL-10 [5, 7, 8]. This evidence concerns the gene TNF and chronic obstructive pulmonary disease.