Numerous studies have shown that cancer is the result of the long-term and repeated effects of various environmental factors on individuals with different genetic qualities. As mentioned above, the proportion of patients with family history of cancer in esophageal cancer is significantly higher than that in the control group, suggesting that there is a genetic predisposition for the development of esophageal cancer and genetic factors may be an important risk factor for its development. Esophageal cancer, also known as esophageal cancer, is a malignant tumor that occurs in the epithelial tissue of the esophagus, accounting for 2% of all malignant tumors. The occurrence of esophageal cancer is related to chronic irritation by nitrosamines, inflammation and trauma, genetic factors and the content of trace elements in drinking water, food and vegetables. China is a high incidence area of esophageal cancer. However, there are more men than women, and most of them are over 40 years old. The following is the introduction of “the relationship between the occurrence of esophageal cancer and heredity”. A large number of studies have shown that cancer is the result of various environmental factors acting repeatedly on individuals with different genetic qualities over a long period of time. As mentioned above, the proportion of patients with family history of cancer in esophageal cancer is significantly higher than that of the control group, suggesting that there is a genetic predisposition for the development of esophageal cancer and genetic factors may be an important risk factor for the development. With the development of molecular biology and molecular genetics, numerous evidences have shown that the malignant transformation of normal cells involves changes in the structure and regulatory control of genetic material, and what is inherited from the previous generation is not the tumor itself, but the susceptibility to tumor. The nature of this tumor susceptibility may be caused by abnormal DNA structure or errors in replication, transcription, or expression in the patient, or may be related to activation of carcinogens, diminished or lost enzyme activity required for harmlessness, or may be the result of congenital or acquired chromosomal aberrations or certain immunogenetic defects. A significantly higher rate of chromosomal aberrations has been observed in members of high-incidence families than in controls. It has been shown that lymphocytes of high-incidence family members are more prone to sister chromatid exchange (SCE) and possible specific fragile sites have been identified on their chromosomes, such as 1p13-p36 and 4q21-q31, which may play certain important synergistic roles in esophageal carcinogenesis. It has been found that familial susceptibility to esophageal cancer is related to familial immunodeficiency, and certain immune functions of patients with a family history of cancer and their relatives are significantly lower than those of controls without cancer families, and patients and their relatives mostly have similar immune function defects. Whether this immune dysfunction is genetic or environmental is yet to be further investigated.