S100A9 and myocarditis: Furthermore, compared with myocarditis mice, the mRNA levels of RAGE and Dia‐1 were significantly reduced in the hearts of CVB3‐infected S100A9−/− mice, while there was no statistical difference in MyD88, indicating that CVB3 may induce myocarditis by activating the S100A9‐RAGE‐Dia‐1 pathway, and defective S100A9 gene leads to the suppression of this axis thereby attenuating myocardial inflammation.62