Objective: To investigate the clinicopathological features, immunophenotype and molecular genetic changes of switch/sucrose non-fermentable complex (SWI/SNF) complex deficient tumors in digestive system, and to analyze the diagnosis and differential diagnosis points. Methods: The clinical data of 31 patients with SWI/SNF complex deficient carcinoma of digestive system were collected. The histological morphology, immunohistochemical results and molecular changes were observed and analyzed. Results: Among the 31 patients, 19 were male and 12 were female, aged 43-80 years, mean age 64 years, median age 66 years. Location of disease: lower esophagus (gastroesophageal junction) 1 case, stomach 7 cases, right colon 3 cases, pancreas 18 cases, ampulla 2 cases. Histologically, 15 tumors were undifferentiated carcinoma, showing diffuse, solid, or nested, streaked, or pseudoglandular pattern of tumor cells, coagulative necrotic areas were seen in most cases. The tumor cells were mainly epithelioid cells with poor adhesion, rich cytoplasm, light staining or eosinophilic, slightly rough or vacuolar nuclear chromatin, obvious nucleoli, pathological mitotic figures were easy to see.16 cases were poorly to moderately differentiated ductal adenocarcinoma, adenosquamous carcinoma or intraductal papillary mucinous tumor (IPMN) with associated invasive carcinoma. Immunophenotype: 14/15 cases of undifferentiated carcinoma showed BRG1 loss expression, 1 case of undifferentiated carcinoma in pancreas showed INI1 partial loss expression, but BRG1 retained expression. CK-pan expression was negative or scattered in 4/15 cases of tumor cells, other epithelial markers were occasional positive or mostly negative in some tumor cells. 7/13 Syn tumor cells were weakly to moderately positive, 2 of them were weakly positive for CD56 or INSM1, and all of them were negative for CgA. BRG1 expression was retained in 16 pancreatic/ampullary carcinomas, INI1 expression was partially lost or decreased in 8 of 16 pancreatic/ampullary carcinomas, and retained in 8 of 16 pancreatic/ampullary carcinomas.22 patients were followed up, 6 patients died. Molecular pathology: SMARCB1 gene mutation was found in 14/16 cases of pancreatic or ampullary cancer, SMARCA4 gene mutation was found in 2/16 cases, KRAS gene mutation was found in all cases, and TP53 gene mutation was found in 14/16 cases. conclusion: SWI/SNF complex deficient tumor is a rare and highly malignant tumor, some of them are undifferentiated carcinomas without specific differentiation features. Extragastrointestinal SWI/SNF complex deficient carcinoma may have more differentiated adenocarcinoma morphology. Understanding its histological and immunohistochemical expression characteristics may suggest the detection of SWI/SNF proteins such as BRG1 and INI1 to reduce missed diagnosis and misdiagnosis. SWI/SNF-related gene mutations were associated with KRAS and TP53 gene mutations in pancreatic cancer.