A 66-year-old woman was resuscitated from a cardiac arrest after completing 1 cycle of cardiopulmonary resuscitation (Supplementary Figure 1). Echocardiography showed severe global akinesia and small pericardial effusion. Coronary angiography was normal. Endomyocardial biopsy was performed. Myocardial pathology confirmed her diagnosis of giant cell myocarditis (GCM) (Figure 1). As a treatment for GCM, she received anti-thymocyte globulin (ATG) followed by cyclosporin A and everolimus (Supplementary Figure 2).¹⁾ Follow-up pathological examination showed resolving myocarditis on the 12th hospital day (Figure 2) at 5 weeks after starting treatment. Histological confirmation is essential for verifying GCM in myocarditis.²⁾ Observations in experimental GCM on Lewis rate model suggest that autoimmune mechanisms medicated by CD4⁺ T lymphocytes are responsible for the pathogenesis of GCM.³⁾ In acute phase, T helper cell type 1 (Th1) is dominant, which may lead to inflammation at the induction of myocarditis. ATG therapy induces a profound decrease in Th1 cell counts.⁴⁾ Early ATG administered seems to play a key role in alleviating the fulminant inflammation of the heart and resulted in a better clinical course.