In RA, the joint microenvironment undergoes an upregulation of various cytokines and chemokines, such as Interleukin 1β (IL-1β), Interleukin-6 (IL-6), Interleukin-17 (IL-17A), Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF), and Tumor Necrosis Factor-α (TNF-α) (McInnes and Schett, 2007). This evidence concerns the gene TNF and rheumatoid arthritis.