In CVB3-infected S100A8 and S100A9 knockout mice, left ventricular function improved and cardiac inflammatory and oxidative response decreased compared with those in wild-type CVB3-infected mice [93], suggesting that in addition to NETs, S100A8 and S100A9 derived from neutrophils play a key role in inducing myocarditis. Here, S100A9 is linked to myocarditis.