The prevalence of endometrioid histology in adenomyosis-associated ovarian cancers may be explained by the shared origin of endometrial-type tissue and common molecular alterations, including ARID1A mutations and PI3K/AKT pathway activation, which are frequently observed in both endometriosis-associated and adenomyosis-associated malignancies [13, 14]. This evidence concerns the gene AKT1 and endometriosis.