Abstract: Endometrial cancer (EC) is a common malignant tumor within the female reproductive system, and its incidence is increasing. The prognosis for patients with early EC is good, but the prognosis for patients with advanced and recurrent EC is extremely poor. In recent years, immune checkpoint inhibitors have shown significant promise in tumor therapy, including therapy for patients with advanced and recurrent EC. Some of these patients experience disease progression during immunotherapy, and the mechanism of tumor immune escape is not thoroughly understood. Indoleamine 2, 3-dioxyfenase-1 (IDO1) catalyzes the conversion of tryptophan to kynurenine, which is the first and rate-limiting step in the major pathway of tryptophan catabolism. IDO1 overexpression in a tumor microenvironment results in tryptophan depletion and kynurenine metabolites overproduction, facilitating cancer immune escape. We review the primary mechanisms by which the IDO1 pathway facilitates immune escape in EC, and describe research progress into EC therapy targeting the IDO1 pathway.