Overactivation of the nuclear factor κB (NF-κB) pathway by the STK IκB kinase (IKK) leads to the excessive production of proinflammatory cytokines [e.g., tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β)], exacerbating conditions such as rheumatoid arthritis [116,117]. This evidence concerns the gene TNF and rheumatoid arthritis.