The influence of checkpoint inhibitors on the balance between activation and inhibition of T-lymphocytes is strong. The development of checkpoint inhibitors has led to treatments for many malignancies but has also facilitated auto-immune disease. These immunotherapeutic agents could exacerbate already present autoimmune disease or could cause new complications in patients with no prior history of autoimmunity. Monoclonal antibodies targeting immune check points, namely anti-CTLA4 or anti-PD-1/PD-L1, are generally well tolerated; however, treatment with these drugs is associated with a variety of adverse events, such as cardiotoxicity, among others. The main mechanism of cardiac damage is lymphocytic myocarditis, which can consequently cause many symptoms of cardiovascular disease – from asymptomatic elevation of cardiac markers, heart failure, and arrhythmias to cardiogenic shock. Other adverse events include pericardium damage or Tako-tsubo cardiomyopathy.