While Scgb3a2-transgenic lungs exhibited no phenotypes with normal lung function, they showed exacerbated fibrosis at 3 weeks after subjected to the BLM-induced pulmonary fibrosis model as determined by lung histology, hydroxyproline content, inflammatory cell numbers, collagen gene expression, and inflammatory cytokine levels. This evidence concerns the gene SCGB3A2 and pulmonary fibrosis.