We also found that the feedback of Nrf2 in the lung tissue of the BPD group decreased during the P5 hyperoxia maintenance period, suggesting that the antioxidant capacity of the BPD group decreased; however, the level of HO-1, one of the downstream factors, increased unexpectedly, indicating that there was an imbalance of oxidative stress homeostasis in the BPD group, possibly because of the upregulation of HO-1 protection caused by other pathways. The gene discussed is HMOX1; the disease is bronchopulmonary dysplasia.