In hyperoxia-induced bronchopulmonary dysplasia (BPD) models using neonatal rats, caffeine restored oxidative balance by normalizing lipid peroxidation to normoxic levels, upregulating Nrf2 expression, and inhibiting its negative regulator Kelch-like ECH-associated protein 1 (Keap1), thereby reinstating SOD1 antioxidant function (108). The gene discussed is SOD1; the disease is bronchopulmonary dysplasia.