However, it is recognized in a recent study that Th17 cells can acquire a Th1 phenotype (Th17/Th1) [55], evolve into IFN-γ-producing T cells, and secrete the pro-inflammatory cytokines TNF-α, IL-1-β, and IL-17 [53, 55], thereby exacerbating the proinflammatory state of SLE and leading to the persistence of chronic inflammation in the context of autoimmune disease. The gene discussed is IFNG; the disease is systemic lupus erythematosus.