This is because the metabolism of alcohol in the human body is completed by acetaldehyde deoxygenase 2 (ALDH2), the function of acetaldehyde deoxygenase 2 in the human body is to oxidize acetaldehyde into non-carcinogenic acetic acid, which is eventually broken down into harmless carbon dioxide and water and discharged from the body. However, when the normal gene of acetaldehyde deoxygenase 2 is mutated, the enzyme becomes inactive, resulting in a six-fold increase in the concentration of acetaldehyde in the blood after drinking alcohol, and long-term alcohol abuse will lead to the accumulation of acetaldehyde in the body, which is toxic and may increase the risk of liver cancer. The results of one study found that among those with enzyme activity deficiency, the risk of liver cancer was 3.51 times higher for those who drank more than 3 kg of alcohol per month than for those who were normal gene carriers and did not drink; as the total amount of alcohol consumed by the former increased over their lifetime, their risk of liver cancer showed a significant upward trend. Although alcohol consumption is not the main cause of liver cancer, heavy drinking and high alcohol consumption may lead to alcoholic liver, which may gradually develop into liver cancer, so less alcohol should be consumed to prevent liver cancer. Carriers of acetaldehyde deoxygenase 2 gene variant tend to have neurological symptoms such as flushing, nausea and tachycardia after drinking alcohol. Therefore, if you have these symptoms after drinking alcohol, you should be alert and quit drinking or minimize the intake of alcohol to prevent the occurrence of liver cancer.