Pancreatic cancer is genetically linked, as confirmed by two points: first, the process of pancreatic tumorigenesis is accompanied by the accumulation of dominant mutations, and second, those individuals who have inherited genetic mutations are at higher risk of developing pancreatic cancer. There are four types of genes involved in pancreatic cancer development: oncogenes, oncogenes, genome maintenance genes and tissue maintenance genes. Some of the gene mutations are inherited from the family line, called germline mutations, and some are acquired mutations that cause tumorigenesis in tissues and are not passed on to offspring, called somatic mutations. The initial reports of familial occurrence of pancreatic cancer were case reports of multiple members of the family developing pancreatic cancer. For example, in 1973 MacDermott and Kramer reported the development of pancreatic cancer in four siblings in a family, and in 1982 Dat and Sontag reported one case of pancreatic cancer in a brother. Ehrenthal et al. reported a family line with three generations of pancreatic cancer. lynch was probably the first to cite a large number of familial cases of pancreatic cancer and hypothesized the existence of an autosomal dominant mode of inheritance in some families. However, to date, the idea that there is familial inheritance of pancreatic cancer has not been widely accepted. Several epidemiologists have conducted studies surrounding the familial development of pancreatic cancer, and these studies have demonstrated that the incidence of pancreatic cancer is 3-13 times higher in those with a family history of pancreatic cancer than in those with an epidemic, and that pancreatic cancer has a tendency to cluster in some families. Genetic syndromes associated with an increased risk of pancreatic cancer are: familial atypical multiple nevi, malignant melanoma, breast cancer, hereditary non-polyposis colorectal cancer, familial pancreatitis, and Peatz-Jeghers syndrome. Patients with these syndromes have the same mutated genes as pancreatic cancer. Although the increased risk of pancreatic cancer in members of families with aggregated-onset pancreatic cancer is well established, how to deal with it is unclear. Prophylactic surgery is an option, but total pancreatectomy leads to diabetes and significant post-surgical complications, and a more reasonable response would be to screen at-risk family members to detect those with early, potentially treatable pancreatic cancer. Unfortunately, however, available serum markers, such as Ca199, are not sensitive and specific enough to be used for screening , and some experts recommend the application of laparoscopic ultrasound combined with abdominal CT scan for screening of high-risk family members. With advances in molecular biology and increased knowledge of pancreatic cancer genetics, molecular genetic screening may be used for early pancreatic cancer detection in the near future.