AMD pathogenesis is highly dependent on oxidative stress, and SOD1 deficiency has been shown to cause dry AMD in a mouse model.[42] Notably, our previous proteomic analysis of human RPE tissue identified high levels of SOD1 as well as elevated glutathione peroxidase (GPX1 and GPX4), PRDX1, PRDX2, PRDX3, and vitronectin (VTN) in the foveomacular retina of the RPE compared to other regions.[13] This difference in the levels of these proteins between the retina and RPE-choroid complex at the foveomacular region may be explained by differences in the molecular function of these tissues. The gene discussed is SOD1; the disease is dry age related macular degeneration.