A 42-year-old, previously healthy Sri Lankan man presented with low-grade fever, upper respiratory symptoms, and fatigue of 1-week duration. Investigations revealed elevated liver enzymes: aspartate aminotransferase (AST) 117 U/L and alanine aminotransferase (ALT) 186 U/L. There was no history of jaundice, pruritus, or alcohol use. An ultrasound scan of his abdomen showed grade 1 fatty liver with no liver parenchymal changes. Viral screening for hepatitis A, B, and C were negative. Serum ferritin was 1292 μg/L. Full blood count was normal, including hemoglobin (Hb) 147 g/L, white blood cells (WBC) 6.5 × 109/L, and platelets 213 × 109/L; C-reactive protein (CRP) was 4.8 mg/dL, total bilirubin was 15.9 μmol/L, total protein was 74 g/L, and albumin was 44 g/L, which were all normal. Serum ferritin repeated in a month, after complete resolution of the illness, was 1103 ng/mL, with a transferrin saturation of 75%, and liver enzymes remained moderately elevated (AST 83.4 U/L, ALT 155 U/L). There was no consanguinity in his parents and no family history of HH. Investigation in regards to inherited iron loading conditions were considered after excluding secondary causes of iron overload. Genetic testing for p.H63D and p.C282Y mutations in the HFE gene by DNA extraction, allele-specific polymerase chain reaction (PCR), and agarose gel electrophoresis showed that he was homozygous for the H63D mutation. A liver biopsy showed increased hepatocellular iron content and features of steatohepatitis. Investigations to assess complications of iron overload, including fasting blood sugar, electrocardiography, and two-dimensional echocardiography, were normal. He was started on venesections. Following two venesections done 2 weeks apart, his liver enzymes started to decline slowly (AST 76 U/L, ALT 151 U/L), serum ferritin came down to 200 μg/L, and transferrin saturation to 26%.