For example, the protein levels of CCL5, IL-6, IL-8, IL-1β, S100A8, ANGPTL4, and VEGFA were increased in chondrocytes, cartilage, synovium, or synovial fluid derived from OA patients, which in turn stimulated the expression of MMPs [36–44]; the expression of IL-7R was elevated in RA FLSs and blockade of IL-7R reduced joint inflammation and cartilage destruction [45, 46]; PTGS2/Cox-2 is a key molecular target for the management of arthritis pain [47]. The gene discussed is CCL5; the disease is rheumatoid arthritis.