An imbalance between T helper (Th)1 cells/Th2 cells and Th17 cells/Treg cells was reported to play a critical role in the breakdown of immune tolerance and prompt the development of AIDs with local production of cytokines (including IFN-γ, TNF-α, IL-21, and IL-17A), including RA, systemic lupus erythematosus (SLE), Sjogren’s syndrome (SS), and autoimmune thyroid diseases (AITD) (27–32). This evidence concerns the gene IFNG and systemic lupus erythematosus.