The clear role of Th2 cells is still to be clearly determined, but a recent study describe that, in advanced stages of EAM myocarditis, Bcl2-like protein (Bcl2L)12, by complexing the master regulator of Th2 differentiation GATA3, favors Th2 cells differentiation by IL-4 expression and blocks Th2 apoptosis inhibiting the expression of p53, leading to a Th2-mediate inflammation in the heart [127]. This evidence concerns the gene IL4 and myocarditis.