Additionally, our group has previously shown that CC16 deficiency leads to dramatically altered pulmonary function and enhanced airway remodeling (7) and that, by binding to the integrin Very Late Antigen-4 (VLA-4) on leukocytes, CC16 can reduce leukocyte adhesion to endothelial cells, lung infiltration, and airway inflammation (8). This evidence concerns the gene SCGB1A1 and inflammatory response.