The mutation signature is concordant with type I endometrioid carcinomas, which are preferentially associated with mutations in PTEN (52%–78%), KRAS, CTNNB1 and PIK3CA, whereas type II serous carcinomas frequently harbor TP53 (60%–91%) mutation and HER2 amplification22. This evidence concerns the gene PTEN and endometrioid adenocarcinoma.