Previous studies have demonstrated that pro-inflammatory cytokines interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) can promote angiogenesis in choroidal neovascular membranes [3, 4], and are able to disrupt the structure and function of the outer and inner blood-retinal barrier (BRB) [5–7], leading to the progression of wet AMD. This evidence concerns the gene TNF and wet macular degeneration.