Not only does overexpression of TGF-β during early neonatal lung development contribute to experimental BPD, but very low levels of TGF-β activity can result in aberrant lung development with altered cell proliferation, alveolar enlargement, and emphysematous changes in the lung parenchyma (Colarossi et al., 2005), which strongly suggests that TGF-β expression needs to be tightly regulated to preserve normal lung development and prevent lung disease. The gene discussed is TGFB1; the disease is bronchopulmonary dysplasia.