Endometrial atypical hyperplasia (EAH) is a commonly occurring precancerous lesion of the endometrium. The standard treatment for EAH is total hysterectomy with bilateral salpingo-oophorectomy. However, although it effectively increases the probability of EAH survival, this treatment is devastating for young women as they would no longer be able to carry a pregnancy. Conservative management for patients with EAH who desire to preserve their fertility has shown encouraging treatment and reproductive outcomes. However, this procedure is not always effective. Approximately 30% of patients are unresponsive to progestogen therapy [1]. In addition, there is a high disease relapse rate after regression, suggesting the existence of an EAH subtype with intrinsic or emergent progestin resistance, the identification of which is essential. Multiple clinicopathological factors have been investigated as potential indicators of progestin response in EAH and EC; however, most studies have reported nonsignificant or conflicting results. The emergence of molecular classification of EC has shed light on the specific fertility-preserving treatment for patients with EC [[2], [3], [4]]. Molecular markers, such as mismatch repair deficiency (MMR-d) and abnormal p53 expression (p53abn), may be used to identify women with EC who may benefit from progestin treatment [3,5]. EAH and EC share similar features in many perspectives. Thus, MMR-d and p53abn can also be applied to stratify women with EAH. As such, this study aimed to evaluate the prognostic value of MMR-d and p53abn in patients with EAH who underwent fertility-preserving treatment.