Currently, it is believed that TLR preconditioning can alter TLR signaling pathways after ischemia, mainly manifested as the activation of the TLR4/TRIF signaling pathway and the inhibition of the TLR4/MyD88 signaling pathway, thereby increasing the production of anti-inflammatory cytokines, reducing the generation of pro-inflammatory cytokines [81], and reducing the inflammatory damage of cerebral ischemia. The gene discussed is MYD88; the disease is ischemia.