Since TRIM29 deficiency restricts cardiotropic viruses by reducing PERK-mediated ER stress and apoptosis and unleashing ROS-mediated type I IFN production in vitro, we delved into the role of TRIM29 in controlling the pathogenesis of viral myocarditis in vivo using a CVB3-induced myocarditis mouse model. This evidence concerns the gene TRIM29 and myocarditis.