It is generally believed that SLE is associated with abnormal cytokine levels, including increased T helper cell type 1 (Th1) cytokine [interferon (IFN)-γ], Th2 cytokine [interleukin (IL)-4], which stimulate antibodies production, and Th17 cytokines (e.g., IL-17) as well as inflammatory IL-1β, IL-6 and IL-18 that may contribute to the pathogenesis of SLE [2,3,4,5,6]. This evidence concerns the gene IFNG and systemic lupus erythematosus.