The exaggerated immune response that characterizes sarcoidosis pathogenesis isdriven by the activation of T lymphocytes and the formation of granulomas [11].Antigen-presenting cells, such as macrophages and dendritic cells, process andpresent environmental or self-antigens to CD4+ T helper cells, leading to therelease of proinflammatory cytokines, including tumor necrosis factor-alpha(TNF-α), interleukin-2 (IL-2), and interferon-gamma (IFN-γ)[12]. The gene discussed is IFNG; the disease is Granuloma.