Along with our partners, we previously documented that Shp2 played an important role in acute cigarette-smoke-mediated IL-8 overproduction[14], loss of Shp2 in alveoli epithelia induced deregulated surfactant homeostasis, resulting in spontaneous pulmonary fibrosis[15], and Shp2 regulated TGF-β1 production in airway epithelia and asthmatic airway remodeling in mice[16]. This evidence concerns the gene TGFB1 and pulmonary fibrosis.