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Although alcohol intake as well as hepatitis viruses has been associated with hepatocellular carcinoma (HCC), gene–alcohol interactions on HCC risk remain to be elucidated. We conducted a case-control study to examine whether polymorphisms of alcohol dehydrogenase 2 (ADH2) and aldehyde dehydrogenase 2 (ALDH2) modified the HCC risk depending on the amount of alcohol intake.ADH2andALDH2genotyping was performed by a duplex polymerase chain reaction with confronting two-pair primers in 209 newly diagnosed HCC cases and 2 different controls [275 hospital controls and 381 patients with chronic liver disease (CLD)]. Multiple logistic regression analyses revealed that heavy drinkers consuming ≥3 “go”s/day of sake (69 g of ethanol/day) showed an increased risk of HCC based on comparison of HCC cases with hospital controls [adjusted odds ratio (OR) = 13.5; 95% confidence interval (CI) 3.3–54.3] or CLD patients (adjusted OR = 7.0; 95% CI 2.5–19.2), whereas the overall risk was not elevated among light to moderate drinkers consuming <3 “go”s/day. Interestingly, light to moderate drinking was associated with an increased risk among those withALDH2*1/*2(adjusted OR = 4.5 or 2.0), but not among those withALDH2*1/*1(adjusted OR = 0.8 or 1.0;pinteraction = 0.03 or 0.13). However, this gene–alcohol interaction was not observed for heavy drinking. Among light to moderate drinkers, people with the combination ofALDH2*1/*2andADH2*2/*2revealed the highest risk of HCC. These findings indicate that theALDH2polymorphism may modify HCC risk among light to moderate drinkers.