The pathogenesis of RA relies on an inflammatory response in the synovial space that is characterized by T helper type 1 cell infiltration with the further release of different cytokines, such as IL-6, TNFα, IL-1β, IL-12, IL-17, and GM-CSF; production of autoantibodies, like rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACPA), by B cells; and cytotoxic CD8 T cell activation [2]. Here, IL1B is linked to rheumatoid arthritis.