IFNG and rheumatoid arthritis: IFN‐γ‐induced activation of macrophages and several inflammatory cells contribute to elevated production of pro‐inflammatory cytokines and disruption of homeostatic regulation.[16] In the meantime, it's reported that inflammatory response amplifier IL‐17 can also contribute to joint damage in RA through mechanisms involving the induction of tissue‐degrading enzymes, synovial pannus expansion, osteoclast formation, and angiogenesis and induces neutrophil extracellular trap formation, promoting the pathogenesis of SLE.[17]