HMGB1/TLR4 signalling via regulating the process above, could affect the distribution of DCs in the myocardium, induce the activation and maturation of DCs, stimulate the expression of costimulatory molecules and promote the release of inflammatory factors through the MyD88/NF‐κB pathway to participate in MI/RI and aggravate myocardial injury. This evidence concerns the gene HMGB1 and myocardial infarction.