Excessive and prolonged activation of immune cells, such as T and B lymphocytes, and overexpression of the master pro-inflammatory cytokine tumor necrosis factor alpha (TNF), together with other mediators such as interlukin-6 (IL-6), interlukin-1 (IL-1), and interferon gamma (IFN-γ), play a central role in the pathogenesis of autoimmune inflammatory responses in rheumatoid arthritis (RA), inflammatory bowel disease (IBD), Crohn’s disease (CD), and ankylosing spondylitis (AS) (Moudgil and Choubey, 2011; Sticherling, 2016; Ellis and Braley-Mullen, 2017). This evidence concerns the gene IL1B and rheumatoid arthritis.