The timing of fetal lung maturation is influenced by endogenous corticosteroids and is accelerated by glucocorticoid treatment. Other hormones have permissive or synergistic effects with glucocorticoids (e.g., thyroid hormones and activators of adenylate cyclase), indicating that lung development is under multi-hormonal regulation. Glucocorticoids affect both lung structure and differentiation of the surfactant system through actions in mesenchymal and epithelial cells. These effects are mediated through glucocorticoid receptors and involve gene activation with de novo synthesis of proteins. The number of inducible (for repressible) proteins is limited to -2% of total proteins, consistent with glucocorticoid effects on specific genes. Although some glucocorticoid-responsive proteins are known (enzymes of phospholipid synthesis and the antioxidant system; surfactant associated protein), the identity of function of most target proteins awaits further research.