In the inflamed RA synovium, activated FLSs adopt an apoptosis-resistant and aggressive proliferative phenotype leading to pannus formation with production of pro-inflammatory cytokines (e.g., TNF-α, IL-6 and IL-1β) and chemokines (e.g., IL-8, CCL2, CCL5 and CXCL10), extracellular matrix-degrading enzymes and pro-angiogenic factors resulting in chondrocyte apoptosis, cartilage matrix degradation and activation of endothelial cells [35,36,52]. This evidence concerns the gene CXCL8 and rheumatoid arthritis.