Indeed, previous studies indicate the effects of Nrf2 on molecular processes of alveolarization and lung diseases of premature births: deficiency in Nrf2 and exposure to hyperoxia in newborn mice increases mortality and the severity of alveolar growth inhibition, and transcriptome analysis of immature lung tissue suggests that the protection against O2 toxicity of Nrf2 may be mediated by its regulation of the cell cycle, metabolism processes, cell–cell interactions, and redox homeostasis [47, 48]. This evidence concerns the gene NFE2L2 and lung disorder.