After their activation, the production of independent or interoperable inflammatory factors including TNF and interleukin and hypoxia-inducing factors, triggering inflammatory storms to exacerbate the immune response, promote synovial cell proliferation and fibrosis, gradually forming vascular fins and damaged cartilage and promoting the development of RA [38,39,40,41]. The gene discussed is TNF; the disease is rheumatoid arthritis.