IRAK4 and viral myocarditis: Valaperti et al. found that after CVB3 infection, TLR7-stimulated IRAK4−/− mice exhibited significantly upregulated STAT5 phosphorylation and enhanced IFN-α and IFN-β expression compared with that of IRAK4+/+ mice, indicating that IRAK4 accelerates viral myocarditis progression by inhibiting TLR7-mediated IFN production [47].