YAP overexpression disrupted the interaction between TAK1 and its downstream proteins IKKα and IKKβ, attenuating the activation of NF-κB signaling which played a major role in osteoarthritis pathogenesis via mediating the expression of proinflammatory cytokines such as TNFα (tumor necrosis factor α), IL-1β and IL-6 (88). This evidence concerns the gene NFKB1 and osteoarthritis.