The clinical manifestations and pathogenic mechanisms of AS and RA vary across different studies.[2,3] RA primarily affects peripheral joints, with synovial inflammation and articular destruction mainly driven by pro-inflammatory cytokines such as tumor necrosis factor (TNF-α), which promotes synoviocyte proliferation, inflammatory mediator release, and osteoclast activation, and IL-6, which induces acute-phase reactants (e.g., C-reactive protein [CRP]), B-cell activation, and osteoclastogenesis. This evidence concerns the gene TNF and rheumatoid arthritis.