In lupus-prone mice, similar to the case for Th17 cells, the IL-23/IL-17 axis plays an important role in the pathogenicity of DN T cells, as these cells lead to systemic inflammation and organ damage in SLE by producing the inflammatory cytokine IL-17 and inducing anti-DNA autoantibody production (9, 37, 80). The gene discussed is IL17A; the disease is systemic lupus erythematosus.