The results of laboratory research performed in mouse models suggest that the NFE2L2/ARE signaling cascade is the most promising target for pharmacological intervention in AMD since NFE2L2 participates in the maintenance of mitochondrial homeostasis and NFE2L2 activators are capable of modulating the processes of mitochondrial biogenesis and mitophagy [10]. The gene discussed is NFE2L2; the disease is age-related macular degeneration.