IL1B and rheumatoid arthritis: In RA pathogenesis, the infiltration of macrophages, B-cells, and T-cells, along with resident fibroblasts, aggravates the inflammatory response by overproducing inflammatory cytokines (IL-1β, IL-6, IL-17a, and TNF-α) and prostaglandin E2 (PGE2) and suppressing anti-inflammatory mediators (IL-4, IL-10, and IFN-γ), which ultimately causes synovial hyperplasia, synovitis, and the erosion of cartilage and bone via disturbing the OPG/RANKL balance [6,7].