If the Nrf2 pathway does not properly function, antioxidative protection would be weaker and oxidative stress would cause severe cell damage. Nrf2−/− mice developed ocular pathology similar to the cardinal features of human AMD; deregulated autophagy is a likely mechanistic link between oxidative injury and inflammation [35]. Nrf2−/− RPE cells are susceptible to oxidative stress induced by t-butylhydroperoxide [32]. This evidence concerns the gene NFE2L2 and age-related macular degeneration.