Among the pro-inflammatory and profibrotic cytokines involved in IPF pathogenesis, interleukin (IL)-1 (4), IL-1β (5), IL-4, IL-5 (6), IL-6Rα (4), angiogenic IL-8/CXCL-8 (7), IL-13, its receptor IL-13 Rα2 (8), and IL-33 (9) have been implicated in accelerated inflammation and irreversible damage to lung architecture with loss of alveolar-capillary barrier basal membrane leading to persistent fibrosis. This evidence concerns the gene CXCL8 and idiopathic pulmonary fibrosis.