In most non-infectious uveitis, including BD, the amplification of the innate immune response and differentiation of CD4+ T lymphocytes to Th1/Th17 lymphocytes stimulate the production of proinflammatory interleukins (TNF-alpha, IL-6 or IL-17) that lead to blood–retina barrier breakdown and the accumulation of fluid in the macular space [37,38]. The gene discussed is TNF; the disease is Behcet disease.