Oxidative stress in a murine BPD model using postnatal hyperoxia (P0 to P4) followed by short-term recovery (14 d) in normoxic conditions was associated with significantly increased mRNA expression for antioxidant genes (e.g. HO-1 and Sod) mediated by Nrf2 [57]. The gene discussed is HMOX1; the disease is bronchopulmonary dysplasia.