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. This evidence concerns the gene CTLA4 and Ventricular arrhythmia.