The author proposed that locally increased TNF-α might cause apoptosis of profibrotic macrophages, important in pathogenesis of pulmonary fibrosis through secretion of TGF-β1, IGF-1, PDGF, and arginase I. These microphages could also contribute to the pool of myofibroblasts via trans-differentiation (Gibbons et al., 2011). The gene discussed is TNF; the disease is pulmonary fibrosis.