The increase in the proinflammatory cytokines might be involved in the pathogenesis of nAMD as systemic IFN-γ promotes a shift towards the proinflammatory M1 macrophages [15], IL-1β stimulates retinal inflammation and neovascularization upon entrance to the choroidal vessels following activation by inflammasomes [42], and IL-2 is involved in the migration of retinal pigment epithelial cells and synthesis of extracellular material [44]. The gene discussed is IFNG; the disease is retinitis.