In RA patients, MCP1 (CCL2) and MCP4 (CCL13) are established mediators of synovitis: MCP1 recruits monocytes via CCR2, driving macrophage infiltration and osteoclastogenesis that accelerates joint destruction, while MCP4/CCL13 directly activates fibroblast-like synoviocyte proliferation through extracellular signal-regulated kinase mitogen-activated protein kinase cascade signaling, amplifying cartilage degradation (29, 30). Here, CCL2 is linked to rheumatoid arthritis.