Current evidence suggests that endometrial hyperplasia represents a spectrum of increasingly atypical proliferation of glands and their lining epithelium that is correlated with increasing persistence, recurrence and progression rates, to carcinoma following curettage and/or progestagen therapy. Hyperplasia can be divided into two phases of pathogenetic development. An initial proliferative phase leading to hypertrophy and a second or remodelling phase, characterized by increasing morphokinetic and biochemical alterations of gland cells. Histologically, the proliferative phase is classified into anovulatory, persistent proliferative endometrium and cystic glandular hyperplasia and the remodelling phase, into adenomatous hyperplasia without and with significant cytologic atypia. The histologic subsets can further be classified as mild, moderate and severe hyperplasia according to their respective clinical behaviour. The data suggest, furthermore, that endometrial C.I.S. represents a transitional state between severe hyperplasia and early, invasive adenocarcinoma. From a pathogenetic standpoint, hyperplasia is induced by longstanding, unopposed estrogenic stimulation and its early phase is made of estradiol-sensitive cells. Paralleling the gradual increase in architectural and cytologic atypia, clones of cells are produced that are relatively insensitive to estradiol and have impaired response to growth-control mechanisms. These estradiol-independent cells are presumably susceptible to malignant transformation.