The process of embryo implantation is extremely complex and consists of 3 stages: localization, adhesion and invasion. It occurs within a very limited time and space frame (the so-called “implantation window”) and requires synchronization, interaction and cooperation between the endometrium and embryo development. The mechanisms of embryo implantation are not yet fully understood, but the elements of successful embryo implantation include a high-quality embryo, a receptive endometrium, and an appropriate endocrine environment. In this article, we will describe the effects of endometriosis on embryo fertilization and possible ways to improve the rate of embryo fertilization in patients with endometriosis. I. Effects of endometriosis on embryo fertilization. 1. Effect of endometriosis on oocyte and embryo quality: It was found that if the donor oocytes were from patients with endometriosis, the pregnancy rate and embryo implantation rate of the recipient decreased. Apparently, the decrease in the fertility rate may be due to the impaired quality of oocytes and embryos. The peritoneal fluid can enter the fallopian tube and uterine cavity via the umbilical end, which plays an important role in stabilizing the internal environment for embryonic growth and development. Changes in the composition of the peritoneal fluid can directly affect the embryo, leading to delayed development or even death. It has been found that ectopic endometrium can induce inflammatory reaction in the peritoneal cavity, leading to an increase in the number and activity of macrophages and an increase in the content of many cytokines, prostaglandins and adhesion molecules, among which the peritoneal fluid of patients with endometriosis contains high levels of I L21 and I L26, which are embryotoxic. 2. The effect of endometriosis on endometrial tolerance, the increased level of prostaglandins in endometriosis patients stimulates abnormal uterine contractions, and the amplitude of uterine contractions in endometriosis patients is three times higher than that in non-endometriosis women. The method of improving embryo implantation in patients with endometriosis. 1.Gonadotropin. The use of gonadotropin-releasing hormone agonists (GnRH-a) has so far been confirmed only with ultra-long-cycle GnRH-a therapy. A meta-analysis of nearly 15 years of studies showed that the pregnancy rate was significantly higher after treatment with ultra-long-cycle GnRH-a than in those who did not use the drug, with an OR of 413 (CI: 210-911), suggesting that the use of GnRH2a for 3-6 months before IVF can increase the pregnancy rate 4-fold. 2. Anti-inflammatory therapy. NSAIDS may reduce uterine contractions and improve the chance of embryo implantation. NSAIDS was found to reduce uterine contractions and increase the chance of embryo implantation. In patients with endometriosis, the progesterone receptor (PR) increased approximately twofold after piroxicam treatment, which presumably increased the PR level and normalized uterine contractions after piroxicam treatment. 3. Surgical treatment. Surgical treatment of endometriosis has been shown to improve the natural fertility of patients with endometriosis combined with infertility. Surgical removal of lesions from the abdominal and pelvic surfaces may improve the toxic environment in the pelvic cavity and reduce the chance of rapid growth of the lesions during the superovulation process.