Mo-AMs with M2-like features are thought to be the main source of TGF-β in lung fibrosis (49, 86), but monocytes and monocyte-derived lung macrophages also release other profibrotic factors such as matrix metalloproteinases that are important for the activation, differentiation, and accumulation of fibroblasts, as well as epithelial-to-mesenchymal transition (87) (Fig. 2). The gene discussed is TGFB1; the disease is pulmonary fibrosis.