Implicated in epithelial–mesenchymal transition (EMT) (8), myofibroblast differentiation (9), and epithelial apoptosis (10), TGF-β overexpression may be pathogenic for BPD, emphasizing the critical need for TGF-β regulation during fetal lung development (11). This evidence concerns the gene TGFB1 and bronchopulmonary dysplasia.