The reasons were as follows: first, there was no risk factors such like stress trigger, sepsis or pheochromocytoma; second, cTnI elevated so obviously (above 1, 000 multiple of normal upper limit) [10] and dropped slowly, and the ratio between peak cTnI and EF measured at admission was 95.9 (much higher than cut-off value of ≤60) [11]; third, cardiac MRI showed significant late gadolinium enhancement of subendocardial area in anterior wall [12, 13]. The gene discussed is TNNI3; the disease is hereditary pheochromocytoma-paraganglioma.