Beyond NETosis, neutrophils in synovial joints also contribute to RA pathogenesis by producing cytokines such as TNF and BAFF (B cell‐activating factor), as well as signaling molecules such as RANKL, together with various chemokines and their receptors, which collectively drive local autoantibody production, bone erosion, and sustained inflammation [84]. This evidence concerns the gene TNFSF13B and rheumatoid arthritis.