The importance of IFN-γ priming for the functionality of MSCs/CardAPs on the one hand and the increased cardiac IFN-γ levels in acute CVB3-induced myocarditis on the other hand [127] support the hypothesis that MSCs/CardAPs will exert their protective effects in the cardiac inflammatory environment of acute CVB3-induced myocarditis. This evidence concerns the gene IFNG and myocarditis.