A 56-year-old woman was readmitted to the hospital with abnormal liver function tests, persisting for the last 18 months. Her hepatic markers were as follows, tested 18 months ago: alanine aminotransferase (ALT) 113 U/L, aspartate aminotransferase (AST) 104 U/L, alkaline phosphatase (ALP) 124 U/L, and glutamate aminotransferase (GGT) 78 U/L. This was attributed to a positive HAV-IgM (ELISA, OD value of attributed absorbance >=2.1, determined to be positive). She was diagnosed with acute hepatitis A and hospitalized in isolation for treatment. Abnormal symptoms, such as fever, fatigue, abdominal pain, or yellow urine, were not observed. She was treated with glutathione 0.9 g and glycyrrhetinic acid 150 mg/day for 45 days. The liver function recovered, and the markers were as follows: ALT 56 U/L, AST 43 U/L, ALP 109 U/L, and GGT 65 U/L. However, HAV-IgM was still positive. During this time, anti-nuclear antibodies (ANA) 47 U/L (normal <10 U/L) were also detected. Tests for antimitochondrial antibodies (AMAs) and anti-liver kidney microsomal (LKM) antibodies, and anti-smooth muscle antibodies (SMAs) were negative. The immunoglobulin G (IgG) level was 18.3 g/L (normal range 6.2-16.1 g/L) and the IgM level was 2.71 g/L (normal range 0.98-2.04 g/L). Following discharge, regular monthly reexamination showed abnormal liver function with repeated fluctuations (Figure 1). The patient developed fatigue, decreased appetite, and yellow urine for 15 days, thus indicating recrudescence. Liver function tests showed abnormal results [total bilirubin (TBIL) 43 mol/L, ALT 452 U/L, AST 254 U/L, ALP 175 U/L, GGT95 U/L]. Further testing revealed the ANA level of 102 U/L, IgG 26.3 g/L, IgM 2.71 g/L, and IgA 5.32 g/L (normal range: 0.76-3.9 g/L). The analysis of a liver biopsy specimen revealed histological changes consistent with typical autoimmune hepatitis. There was moderate to severe interfacial inflammation, numerous lympho-plasma cell infiltrates, lymphocytic penetration, and rosette-like hepatocytes (Figure 2). HAV-IgM was positive. To rule out the possibility of HAV infection, a reverse transcription-polymerase chain reaction (RT-PCR) was conducted to detect HAV RNA in the serum. The analysis of the current samples, as well as those from a year ago, was found to be negative. Clinical diagnosis of AIH was made with a false-positive HAV-IgM. Methylprednisolone 32 mg/day was administered, which was tapered to 20 mg/day after 1 month. The liver function tests, done daily, returned to normal after 2 months, following which, methylprednisolone was further tapered to 8 mg/day as a maintenance treatment. On reexamination, the patient was negative for HAV-IgM and HAV RNA. The tests for Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes simplex virus (HSV), varicella-zoster virus, and adenovirus were negative. There was also no drug-induced liver injury or history of alcohol addiction.