After the imbalance of CD4+T cells in RA patients, their differentiation direction will be toward T helper cell 17 (Th17), where the secreted levels of interleukin-17 (IL-17), interleukin-21 (IL-21), and interleukin-23 (IL-23) will be significantly increased, which will stimulate the production of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-1 (IL-6), prostaglandin E2 (PGE2), and others by fibroblast-like synoviocytes, promote the production of osteoclasts and produce severe synovitis [7]. This evidence concerns the gene CD4 and rheumatoid arthritis.