A 72-year-old Korean male was admitted because of sudden onset of abdominal distension. He had been treated with amiodarone 200 mg, felodipine 5 mg, hydrochlorothiazide 25 mg, and aspirin 100 mg per day for hypertension with atrial fibrillation for 5 years. Before starting medication, he had undergone ultrasonography of the liver and serum biochemical tests including liver chemistry and lipid profile, with all results being within the normal range. There was no evidence of hepatitis B and C, autoimmune hepatitis, or metabolic diseases such as nonalcoholic steatohepatitis, Wilson's disease, hemochromatosis, or α1-antitrypsin deficiency. In addition, he had no history of heavy alcohol consumption. CAD, cationic amphiphilic drug. Physical examination revealed massive ascites, peripheral edema, and splenomegaly. Liver chemistry tests were abnormal: serum albumin = 2.7 g/dL, total bilirubin = 2.3 mg/dL, aspartate aminotransferase = 317 U/L, alanine aminotransferase = 237 U/L, alkaline phosphatase = 137 U/L, gamma-glutamyl transpeptidase = 185 U/L, and international normalized ratio = 1.32. A transthoracic echocardiogram showed mild concentric left ventricular hypertrophy, ejection fraction of 73%, and mild pulmonary hypertension. A precontrast computed tomography scan showed a diffusely hyperdense liver and a large amount of ascites (Panel A). Transjugular liver biopsy demonstrated cirrhosis with polymorphonuclear infiltrate, Mallory bodies (arrows), and ballooning degeneration (arrowheads) (Panel B). Electron microscopy showed lysosomal myeloid bodies with dense deposits (asterisks) within hepatocytes (Panel C). On the basis of clinical history and histologic findings, amiodarone-induced liver cirrhosis was diagnosed, and the drug was replaced with another antiarrhythmic agent (propafenone). He was discharged with improved general condition with marked reduction of ascites. Although asymptomatic elevations of aminotransferases have been reported in up to 25% of the patients treated with long-term amiodarone therapy, symptomatic liver dysfunction has been reported to occur in fewer than 1% of these patients.1, 2 However, amiodarone-induced hepatitis can progress to cirrhosis, resulting in decompensated hepatic failure, although this rarely happens.1, 2 Amiodarone is one of the cationic amphiphilic drugs (CADs) that can cause phospholipidosis in liver.3 In this case, the findings demonstrating intralysosomal myelin figures and electron-dense material on electron microscopy are compatible with the findings of CAD-induced phospholipidosis.4 However, the functional consequences of phospholipidosis on cellular or tissue function have not been well explained. Rather, liver damage is considered to be caused by amiodarone-induced inhibition of mitochondrial β-oxidation.5