Whereas CTNNB1-activating mutations have long been recognized as a driving mechanism of EMT in multiple cancer types, including uterine endometrioid carcinoma40, in the current CS cohort and contrary to our expectations, the mutational status was independent of the EMT score but, instead, associated with hypomethylation of the miR-200a/200b/429 and miR-141/200c promotors. Here, CTNNB1 is linked to Cowden syndrome 1.