Differential PTEN and ARID1A expression between eutopic endometrium and cystic adenomyomas supports a model in which PTEN‐deficient endometrial clones invade the myometrium to form adenomyosis, with additional ARID1A loss and pAKT activation driving cystic enlargement without malignant transformation. The gene discussed is PTEN; the disease is adenomyosis.