Extensive basic and translational research indicates that the Nrf2/HO-1 pathway exerts protective effects through multiple mechanisms: reducing reactive oxygen species (ROS) levels, inhibiting nuclear factor-kappa B (NF-κB)-mediated inflammation, regulating macrophage polarization, and influencing processes such as apoptosis, ferroptosis, and fibrosis, thereby significantly alleviating tissue damage and clinical symptoms in arthritis. The gene discussed is NFKB1; the disease is arthritic joint disease.