In conclusion, these findings underscore the critical role of PD-1 signaling in maintaining cardiac integrity and regulating immune responses in various models of myocarditis and cardiotoxicity, while inflammatory processes, the interaction of immune cells (e.g. T cells) and immunomodulatory substrates (e.g. TNF-α and IFNγ) present as the driving factors for the induced phenotype. This evidence concerns the gene TNF and myocarditis.