During the pathogenesis of RA, the expression of IL-23 promotes Th17 cell proliferation and IL-17 production, which in turn upregulates TNF-α, IL-1β, and RANKL in RA fibroblast-like synovial cells (RAFLS), forming the IL-23/IL-17/NF-κB inflammatory signaling axis, which further exacerbates synovial inflammation and joint destruction. This evidence concerns the gene IL17A and rheumatoid arthritis.