VPA attenuated the clinical severity of Coxsackie B3 virus (CVB3) myocarditis, and mortality from CVB3-induced myocarditis of BALB/c male mice, decreased the percentage of splenic Th17, increased the rate of Treg cells, downregulated the IL-17A expression, upregulated IL-10 in serum and heart tissues of CVB3 infected mice, inhibited the differentiation of the Th17 cells and promoted the differentiation and suppressive function of Treg cells [122]. This evidence concerns the gene IL17A and myocarditis.