Bone erosion in RA is the result of multiple cellular interactions: in the initiation phase, the interaction is shown as “abnormal T-B cell contact → autoantibody + Th17 activation → synovial inflammation”; and in the amplification phase, it is expressed like “macrophage M1 polarization, FLSs activation, NETs release → TNF-α/IL-6/IL-17 storm→RANKL/OPG imbalance”; while in the Terminal phase, it is manifested as “hypoxic microenvironment + MMPs + OC overactivation→cartilage degradation and bone resorption”. This evidence concerns the gene IL6 and rheumatoid arthritis.