Following the injury in the alveolar epithelium, recruited macrophages can contribute to the pathogenesis of pulmonary fibrosis via the secretion of a plethora of mediators such as cytokines, interleukins, transforming growth factor beta (TGF-β), connective tissue growth factor (CTGF), epidermal growth factor receptor (EGFR) ligands, and proteases [10,11,12]. The gene discussed is CCN2; the disease is pulmonary fibrosis.