A 51-year-old woman was admitted to our emergency department due to hemodynamically stable ventricular tachycardia (VT). Her family history was unremarkable for cardiovascular disease, sudden death, or other inherited disorders. Apart from a long history of arrhythmias, she had no special medical or psychosocial record. The patient experienced recurrent paroxysmal palpitations since she was 15 years old. In her 30s, she was diagnosed with Wolff–Parkinson–White (WPW) syndrome () with paroxysmal supraventricular tachycardia, for which she received her first radiofrequency catheter ablation (RFCA). Echocardiography at that time showed a normal heart, while cardiac troponin levels were not tested. Three years ago, she was admitted with paroxysmal atrial flutter (), during which echocardiography revealed an enlargement of the left atrium (45 mm) but normal left ventricular wall thickness (10 mm), chamber size (51 mm), and ejection fraction (EF) (72%). She was discharged after the RFCA for atrial fibrillation (AF) with a normal troponin-T level. This was her third hospitalization for palpitations. Upon admission, ventricular tachycardia () was recorded, which was electrically converted to sinus rhythm with a complete left bundle branch block (). Despite no heart murmurs or abnormalities of other systems found in physical examination, a slightly elevated N-terminal pro-B-type natriuretic peptide (568 pg/mL, normal reference value: 0–227 ng/L), markedly increased troponin-T (168.7 ng/L, normal reference value: 0–14 ng/L), and creatine kinase (1,198 IU/L, normal reference value: 19–226 IU/L) were identified. Echocardiography revealed a slightly dilated left ventricle of 55 mm and a slightly decreased EF of 51%. The LA remained enlarged, but the wall thickness was normal (). Cardiovascular magnetic resonance (CMR) imaging was further performed, which displayed endomyocardial late gadolinium enhancement (LGE) in the anterior, inferior, and lateral walls (). The following whole-exome sequencing (WES) demonstrated a heterozygous variant in lysosome-associated membrane protein 2 (LAMP2) gene (c.696T>A; p.Cys232Ter) (), which is located in coding exon 5 of LAMP2. According to ClinVar records, this mutation changes the amino acid from a cysteine to a stop codon, which is expected to result in an absent or disrupted protein product (). Because of the pathogenic gene mutation with multiple arrhythmias and myocardial involvement, the diagnosis of Danon disease was confirmed. She received the third RFCA, followed by implantable cardioverter defibrillator implantation.