Low dose IL‐2 can reduce the severity of vascular and bone lesions in collagen‐induced arthritis immune model, and inhibit osteoclast formation in vitro by phosphorylation of nuclear factor‐κB (NF‐κB), which inhibits the receptor activator of NF‐κB ligand effect through c‐Jun N‐terminal kinase (JNK) pathway, and its immunotherapeutic effect depends on the activation of JNK. The gene discussed is IL2; the disease is arthritic joint disease.