In OLP, Ge et al. (2012) demonstrated that the activation of TLR4 initiated a signaling cascade that resulted in the induction of NF-κB, which controls the release of proinflammatory cytokines and chemokines, suggesting that the TLR4 and NF-κB signaling pathway may be associated with the perpetuation processes of OLP [23]. The gene discussed is TLR4; the disease is oral lichen planus.