Disruption of IL-6 regulation has been demonstrated to play a crucial role in pathogenesis of rheumatoid arthritis [3, 4], including promoting leukocyte recruitment to the site of inflammation [5], helping naive T cell differentiation to T helper 17 cells [6], stimulating osteoclast maturation and activation via receptor activator of nuclear factor-Κb ligand (RANKL) [7], promoting angiogenesis by increasing production of vascular endothelial growth factor (VEGF) [8]. Here, VEGFA is linked to rheumatoid arthritis.