The major pathophysiological component of RA is the chronic inflammatory process, which includes multiple systemic changes such as synovial hyperplasia because of increased proliferative cellular infiltrates of leukocytes, an abnormal increase in several pro-inflammatory cytokines (particularly Interleukin 6 (IL-6), Interleukin-1 beta (IL-1β), and Tumor Necrosis Factor Alpha (TNF-α)), consequent cartilage and bone destruction with swelling, deformation, and loss of function of joints [2,3]. This evidence concerns the gene IL1B and rheumatoid arthritis.