Consistently, Wong et al. also found that the proinflammatory cytokine IL-23 and IL-12 can promote the disease severity by activating pathogenic Th1 and Th17 cells via the induction of downstream Th1 chemokine CXCL10 and inflammatory cytokine IL-17 in SLE, demonstrating that the IL-23/IL-17 axis of inflammation and related molecules may arise as a therapeutic target for treating autoimmune disease. This evidence concerns the gene IL23A and autoimmune disease.