Similar to the dualistic pathway of pathogenesis of serous carcinomas, molecular profiling of high-grade endometrioid carcinomas are notable for mutations in TP53 with the absence of other molecular alterations, while low-grade endometrioid carcinomas were strongly associated with microsatellite instability (20%), CTNNB1 mutations (~50%), and KRAS mutations (up to 35%) [135-137]. This evidence concerns the gene TP53 and endometrioid adenocarcinoma.