Studies have demonstrated its ability to inhibit the expression of inflammatory cytokines, such as IL-1β, IL-6, and TNF-α, prevent IL-17A-mediated CCL20 production, suppress P38 MAPK and ERK activity, reduce IL-17 expression, and influence the differentiation of naïve CD4+ T cells into various effector subgroups, thereby aiding in the treatment of autoimmune diseases [37–39]. This evidence concerns the gene IL1B and autoimmune disease.