Although the pathological mechanisms of AMD are not fully understood, many studies have suggested that AMD is an inflammatory process that involves increased production of many inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukins-1β, 6, 8 and 33 (IL-1β, IL-6, IL-8 and IL-33) [1,4], vascular endothelial growth factor A (VEGFA) [5] and activation of the alternative complement pathway [6]. This evidence concerns the gene IL1B and age-related macular degeneration.