This chapter focuses on the precursors of endometrioid and serous cancers. It identifies a spectrum of atypical endometrial glandular and surface changes that were distinct from both the background benign endometrium and the adjacent endometrial clear-cell carcinoma. Endometrial cancers encompass tumors with a range of morphologies that display a spectrum of clinical presentations. Patients on tamoxifen are prone to developing endometrial polyps, hyperplasia and premalignant and malignant endometrioid lesions. Risk of Endometrial intraepithelial neoplasia/atypical hyperplasia and endometrial cancers includes hormonal imbalances and genetic defects. Endometrial cancers and their precursors are known to be driven by increases in estrogen and dampened by relative decreases in progestin. Hyperplasia without atypia tends to be polyclonal and harbors only low levels of somatic mutations in the scattered endometrial glands. From 1% to 3% of patients with ‘untreated’ endometrial hyperplasia without atypia may progress to well-differentiated endometrioid carcinoma.