It is involved in modulating different inflammatory signaling pathways that are central to SLE pathology, including nuclear factor kappa B (NF-κB), suppressor of cytokine signaling 2 (SOCS2), and mitogen-activated protein kinase (MAPK) signaling pathways20–22, and control the expression of proinflammatory cytokines such as IL-17, IL-6, IL-18 and tumor necrosis factor-alpha (TNF-α)23,24. This evidence concerns the gene SOCS2 and systemic lupus erythematosus.