Disturbances of the pulmonary microenvironment induced by TGF-β are critical to promote the recruitment of circulating fibrocytes and bone marrow–derived progenitor cells to the lung (3), and enhance the pro-fibrotic capacities of these cells or induce their differentiation into activated myofibroblasts (4), eventually leading to the typical IPF symptoms like ECM deposition and abnormal collagen accumulation (5). The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.