Experimental NE-AMD induced by SCGx can be divided in two phases: an early phase (up to 6 weeks post-SCGx), characterized by PR dysfunction (ERG a-wave), BrM thickening, decreased RPE melanin content, and RPE65-immunoreactivity, subtle ultrastructural RPE and PR alterations, increase in oxidation markers (4HNE, CML, MitoSOX), and mitochondria mass decrease, followed by a late phase (at 10 weeks post-SCGx), at which severe RPE ultrastructural damage and PR loss become evident, including RPE and PR apoptosis [13]. The gene discussed is RPE65; the disease is age-related macular degeneration.