The etiology and pathogenesis of primary hepatocellular carcinoma have not been determined so far, and it is believed that it is related to a combination of factors, with recent studies focusing on hepatitis B and C viruses, aflatoxins and other chemical carcinogens. Viral hepatitis: clinically, about one-third of primary liver cancer patients have a history of chronic hepatitis. Domestic census found that the incidence of hepatitis is also high in areas with high incidence of primary liver cancer. Epidemiological survey found that the HBsAg positivity rate of people in areas with high incidence of liver cancer is higher than that in low incidence areas, and the serum HBsAg positivity rate of liver cancer patients is significantly higher than that of healthy people. Pathology found that liver cancer combined with cirrhosis is mostly nodular cirrhosis. The latter is closely related to hepatitis. In recent years, the presence of HBsAg in hepatocellular carcinoma cells has been shown by methods such as lichen red staining, and it has also been confirmed that HBV (hepatitis B virus) can be integrated into the DNA of host hepatocytes, and human hepatocellular carcinoma cell lines capable of producing HBsAg have also been established. The above facts indicate a causal relationship between viral hepatitis B and liver cancer. In recent years, the study of what used to be called non-A non-B hepatitis, now named hepatitis C, poses a more serious threat to humans than hepatitis B and is more closely related to cirrhosis and liver cancer. Cirrhosis: The incidence of primary liver cancer combined with cirrhosis is very high, about 50-90% according to domestic statistics, while cirrhosis combined with liver cancer is 30-50%. Liver cancer with cirrhosis is mostly of large nodular nature. This type of cirrhosis is mostly post-hepatitis (post-necrosis) cirrhosis caused by viral hepatitis. Hepatocellular carcinoma may occur in the process of hepatocyte regeneration, i.e., carcinogenesis through hepatocyte destruction – proliferation – heterogeneous proliferation. Liver cancer in European and American countries often occurs on the basis of alcoholic cirrhosis, and it is generally believed that biliary and bruising cirrhosis are not related to the occurrence of primary liver cancer. Aflatoxin: aflatoxin has a strong carcinogenic effect on rats, ducks, guinea pigs and other animals. Animal experiments have proved that aflatoxin B1 is the strongest carcinogen for liver cancer. Epidemiological surveys have found that in some areas with a high incidence of liver cancer, grain and oil, food (such as corn, wheat, soybeans, peanuts, etc.) by aflatoxin B1 contamination is often more serious, and less common in low incidence areas. These all suggest that aflatoxin may be a factor in the prevalence of liver cancer in certain areas, but there is no direct evidence of human liver cancer to date. Recently, it has been reported that epidemiological investigation of aflatoxin has nothing to do with liver cancer, and further research is needed. Other chemical carcinogenic factors: Animal experiments have proved that some chemicals such as nitrosamines and azo benzenes can cause liver cancer in many animals. In the soil and water sources of some areas with high incidence of liver cancer, nitrate and nitrite are found to be high. The relationship between these chemical carcinogens and liver cancer deserves attention and research. Parasitic infection: Chinese branchial schistosomes parasitize small bile ducts in the liver and stimulate the proliferation of bile duct epithelial cells, and some of them can become cholangiocarcinoma, because the various stages from bile duct epithelial cell proliferation to cancer can be seen in the section, so it is believed that such liver cancer is produced by the physical or chemical stimulation of parasitic infection. However, the vast majority of cholangiocarcinomas do not have hepatic schistosome infection, so there may be other causes. In schistosomiasis cirrhosis, the hepatocytes are mostly atrophied without obvious hyperplasia, so it rarely causes liver cancer. Many scholars believe that the cause of family gathering may be due to the vertical transmission of viral hepatitis from mother to child. (2) Trace elements: Trace elements from soil, drinking water, food, human hair and blood in high incidence areas were found to be higher in copper and zinc and lower in key. The relationship between copper, zinc and liver cancer is noteworthy. (C) Malnutrition and nutritional deficiency: Nutrition and tumor is a major topic of human health in the 1990s, which has received the attention of all walks of life. Its role is to accelerate or slow down-cancer in the pro-cancer stage. High-fat and pickled and smoked foods are most closely related to the occurrence of tumors, and it is advisable to eat more vegetables, fruits and mixed grains. Animal experiments have confirmed that high-fat diet, hypoproteinemia, methionine and choline deficiency can cause hepatocyte necrosis, steatosis, hepatic steatosis and liver cancer. If the feed is rich in protein, methionine and B vitamins, the occurrence of liver cancer will be delayed or even not occur.