NFKB1 and myocardial infarction: Necrotic and damaged cells induced activation of TLR (especially TLR4), facilitate IκB kinase phosphorylation through MyD88/TAK1 pathway and finally engage NF-κB p65 and p50, leads to activation of plenty of inflammatory factors, including cytokines, chemokines, adhesion molecules and complement factor B.411 Inhibition of NF-κB has been proved to be associated with decreased reperfusion injury after myocardial infarction.412–414