Similarly, preterm neonates with bronchopulmonary dysplasia exhibit oxidative stress-driven programmed cell death pathways (Notch4/SIRT1/P53/Bax, RIPK3/NF-κB) that impair alveolar development, paralleling transport stress scenarios where pulmonary structural integrity is compromised (58, 59). The gene discussed is BAX; the disease is bronchopulmonary dysplasia.