The primary pathological characteristics include persistent synovitis, a disturbance in osteoblast–osteoclast homeostasis, and dysfunction of immune cells.[19,22] The inflammatory process of arthritis in RA is initiated and perpetuated through a network of interactions involving fibroblasts, osteoclasts, B cells, T cells, neutrophils, and macrophages.[23] Additionally, the onset of RA is also influenced by cytokines, including TNF-α, IL-6, and IFN-γ.[24,25]. The gene discussed is TNF; the disease is arthritic joint disease.