Toll-like receptor 4 (TLR4), an innate immune receptor of bacterial endotoxins, is then accumulated to activate the nuclear factor kappa B (NF-κB) signalling transduction pathway, which was reported to be directly involved in inflammation and apoptosis in the epilepsy model16, myocardial infarction model17 and TBI18. The gene discussed is TLR4; the disease is myocardial infarction.