AKR1B10 has also been found to be overexpressed in human non-small cell carcinoma, liver cancer, breast cancer, oral squamous cell carcinoma and pancreatic cancer, and is involved in the occurrence, development and survival of tumor cells through a variety of mechanisms, including cytotoxic reactive carbonyl compounds Detoxification, enhance the migration and proliferation potential of tumor cells, regulate cellular fatty acid synthesis and lipid metabolism, and participate in the acquisition of multidrug resistance in tumor cells. Here, AKR1B10 is linked to familial pancreatic carcinoma.