In the SLE pathogenesis, diverse cytokines are involved in the onset, progression, and exacerbation of the disease, including interferon-alpha (IFNα), tumor necrosis factor-alpha (TNFα), interleukin (IL) 6, IL-10, IL-12, IL-17, IL-21, IL-27, and B cell-activating factor (BAFF), among others [2,3,4,5,6], highlighting SLE as a complex multi-cytokine disease. This evidence concerns the gene IL27 and systemic lupus erythematosus.