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]. The gene discussed is KRAS; the disease is endometrioid adenocarcinoma.