Given the available studies, we can preliminarily determine that IL-27 signaling could influence RA development by regulating CD4+ T cell differentiation, inhibiting monocytes/macrophages and osteoclasts in the joint cavity, interrupting synovial ectopic lymphoid structure (ELS) interactions with Th17 cells, and regulating RA synovial fibroblast (RA-FLS)-mediated inflammation. The gene discussed is CD4; the disease is rheumatoid arthritis.