KRAS has been shown to be amplified in ovarian endometrioid carcinoma and HGSOC and has been associated with an aggressive phenotype of metastatic uterine endometrioid carcinoma (47, 48), whereas MYC amplifications have been observed in a variety of ovarian cancers, including endometrioid carcinomas (49). Here, KRAS is linked to endometrioid adenocarcinoma.