In breast invasive carcinoma (BRCA), cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), colon adenocarcinoma (COAD), esophageal carcinoma (ESCA), glioblastoma multiforme (GBM), rectum adenocarcinoma (READ), stomach adenocarcinoma (STAD), and uterine corpus endometrial carcinoma (UCES), tumors with a combined MMR deficiency and polymerase mutation displayed a significant hypermutant phenotype than tumors with mutations in the MMR or POL gene sets only. This evidence concerns the gene MRC1 and hyperinsulinemic hypoglycemia, familial, 4.