Mice with a double knockout of ARID1A and PTEN in the uterine epithelium developed a rapidly progressive invasive endometrial carcinoma, while ARID1A deletion alone could not initiate neoplastic transformation, and PTEN-deleted mice developed predominantly intraepithelial epithelial neoplasia which only slowly progressed to early endometrioid carcinoma [61]. The gene discussed is PTEN; the disease is endometrioid adenocarcinoma.