The etiology of endometrial hyperplasia is currently unknown. It is usually believed that long-term estrogen stimulation of the endometrium without progestin antagonism is the cause of endometrial hyperplasia. For example, in adolescent and menopausal women, disorders of the gynecologic endocrine system may lead to ovarian anovulation, and thus the endometrium is under the continuous influence of estrogen. Without progestin antagonism, the endometrium is unable to undergo the transition from the proliferative to the secretory phase and is prone to hyperplasia. Some women undergoing hormone replacement therapy after menopause are also prone to endometrial hyperplasia if they are given only estrogen preparations without progestin. Patients who use tamoxifen after breast cancer surgery are also prone to stimulate endometrial hyperplasia due to the weak estrogen-like effect of tamoxifen. In addition, people who are obese, suffer from polycystic ovary syndrome, diabetes mellitus, hypertension, and functional endocrine tumors are prone to endometrial hyperplasia. Therefore, to avoid endometrial hyperplasia, women should control their weight, have a healthy lifestyle, actively control their blood pressure and blood sugar, and use estrogen and progestin drugs to form an artificial cycle for menstrual disorders so that menstruation is regular and endometrial hyperplasia is not allowed to occur.