A 65-year-old man presented to our cardiovascular department due to fatigue and palpation on exertion during the previous three weeks. He had a medical history of diabetes mellitus and hyperlipemia without hypertension or myocarditis. However, he mentioned that his son had dilated cardiomyopathy (DCM) and ankylosing spondylitis (AS). Examination at admission revealed a blood pressure of 115/69 mmHg and pulse of 82 beats/min. The results of routine blood tests for creatine kinase (CK), CK muscle and brain (CK-MB), troponin T, and thyroid function were all within normal limits. ECG revealed I, aVL, and V4–6 T wave inversion (Figure 1). Ultrasonic cardiography showed that the left ventricular ejection fraction (EF) was 32%, indicating ventricular wall dysfunction. Angiography showed no coronary stenosis. Radionuclide imaging demonstrated myopathy of the anterior, part of the inferior, the posterior, and the lateral apical segments based on reduced radioactivity with a patchy pattern, consistent with DCM (Figure 2A). Cardiac magnetic resonance imaging confirmed the decreased left ventricular motion and late gadolinium enhancement in the septal wall (Figure 2B), confirming the diagnosis of DCM. Based on the patient’s family history of AS, we performed computed tomography examination of the sacroiliac joint and tested for human leukocyte antigen B27 (HLA-B27). Observation of the fused joint and the positive result for HLA-B27 supported the diagnosis of AS. However, we needed to discriminate the familial DCM from AS-induced myocardiopathy. The patient’s mother had experienced sudden cardiac death a few years previously. Among the five children of his older aunt, one had DCM and one had AS, and the two grandchildren of this aunt had AS. Among the six children of his younger aunt, one had