Dysregulated metabolism of the RPE and persistent inflammation have been implicated in the pathogenesis of AMD, involving the production of cytokines such as TNFα, TGFβ2, IL6, and IL1β, which, in turn, exacerbate tissue damage, mitochondrial uncoupling through electron leakage, oxidative stress, fibrosis, and necrosis [33]. This evidence concerns the gene IL1B and age-related macular degeneration.