In rheumatoid arthritis, it has been shown that through the activation of T-cells via the IL-17/IL-23 axis, the subsequent Th17 cells become osteoclastogenic, inducing the expression of receptor activator of nuclear factor-κB ligand (RANKL) on both T-cells and osteoblasts, which in turn activates bone destruction and resorption via osteoclasts [14], with IL-17 levels even predictive of damage progression in patients [15]. Here, IL17A is linked to rheumatoid arthritis.