Collectively, acute MI, ventricular arrhythmias, autoimmune T cell-mediated myocarditis and conduction disease may be triggered by suppressing PD-L1, PD-1, or CTLA-4, and direct inhibition of PD-L1 may inevitably accelerate pre-existing heart disease, and invite noninflammatory cardiomyocyte dysfunction in diseased hearts even in the absence of an immune response. Here, CTLA4 is linked to heart disorder.