Non-endometrioid carcinoma is known a priori to be clinically aggressive and can be readily segregated from its endometrioid counterpart at the time of diagnosis [5] because these two entities exhibit striking difference in histopathological (microscopic) appearance and molecular characteristics such as TP53 mutation, [6] CTNNB1 mutation [7], protein levels of estrogen receptor/progesterone receptor (ER/PR) [8], and gene expression profiling [9]. This evidence concerns the gene ESR1 and endometrioid adenocarcinoma.