Increasing evidence supports a role for SHP2 in inflammation-mediated pulmonary diseases, such as allergic asthma, pulmonary fibrosis, acute lung injury, and chronic obstructive pulmonary diseases.51,52 A high activity of SHP2 in pulmonary eosinophils of asthmatic children and in mice with allergic airway inflammation was associated with the dephosphorylation of p190-A Rho GTPase-activating protein.53 Similarly, fibroblasts from patients with severe eosinophilic asthma showed constitutive activation of SHP2, which resulted in negative regulation of IL-6-induced STAT3 phosphorylation. This evidence concerns the gene PTPN11 and chronic obstructive pulmonary disease.