Activation of the cell causes the phosphorylation of I-kB which is degraded followed by the release of the factor NF-κB, which is introduced into the nucleus of the cell and causes the transcription of many proinflammatory mediators including iNOS, COX-2, and TNF-α and IL-1β, IL-6, and IL-8 [66]; thus, bone erosion and cartilage destruction observed in rheumatoid arthritis are due to overproduction of cytokines and inflammatory mediators. Here, IL1B is linked to rheumatoid arthritis.