In fact, increased levels of inflammatory mediators, such as interleukin-17 (IL-17), interferon-γ (INF-γ), and TNF-α, activated NADPH oxidases (Nox) enzymes and increased reactive oxygen species production, acting a pivotal role in the pathogenesis of arthritis and endothelial dysfunction (34). This evidence concerns the gene IL17A and arthritic joint disease.