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. This evidence concerns the gene TNF and systemic lupus erythematosus.