These observations in in vivo knockout animal models suggest that Nrf2 impairs the occurrence of clinical signs like those of dry AMD leading to GA in humans, and control the inflammatory reaction as well, and are confirmed by immunohistochemistry studies of human-eye sections from patients with AMD showing that Nrf2 expression is reduced in RPE cells above drusen compared to its expression in RPE in healthy areas of the same eyes [63]. This evidence concerns the gene NFE2L2 and dry age related macular degeneration.