Following LPS stimulation, the expression levels of MyD88, p-PI3K, and p-cjun in iOGN−/− BMDMs from mice have also been shown to be lower than that in iOGN+/+ BMDMs, indicating that iOGN on innate immune cells promotes the development of viral myocarditis through the activation of the TLR4-MyD88-mitogen-activated protein kinase (MAPK) pathway [44]. This evidence concerns the gene MYD88 and viral myocarditis.