The role of oxidative stress in the pathogenesis of AMD is supported by observations of an AMD-like phenotype in mice with a genetic deficiency in either superoxide dismutase 1 or 2 (Sod1 [4] or Sod2 [5]) or nuclear factor erythroid 2-like 2 (Nfe2l2) [6]. The gene discussed is SOD1; the disease is age-related macular degeneration.