It suppresses p38 MAPK signaling pathway, and reduces arrhythmogenesis following myocardial infarction, and enhances cardiac function (254, 255).It inhibits the expression of TLR4, MyD88, GM-CSF, IL-1β, TNF-α, and COX-2, and attenuates LPS-mediated TLR4-NF-κB pathway activation (256, 257). This evidence concerns the gene MYD88 and myocardial infarction.