Polycystic ovary syndrome (PCOS) is a common endocrine disorder in women of reproductive age, marked by hormonal imbalances, ovarian dysfunction, and metabolic issues. Although the understanding of its pathophysiology has advanced, its connection to an elevated risk of ectopic pregnancy remains a significant clinical concern. Hormone therapy is a fundamental treatment for PCOS; however, its impact on the uterine tube—specifically on tissue morphology, ciliary activity, and epithelial integrity—as well as on gene expression profiles, is not fully understood. Emerging evidence suggests a potential link between these therapy-induced changes and an increased susceptibility to ectopic implantation. Structural and functional alterations in the tubal epithelium, such as impaired ciliary function, can disrupt regular embryo transport. Concurrently, dysregulated expression of genes critical for tubal physiology and embryo implantation may further elevate this risk. Elucidating the molecular mechanisms through which hormone therapy influences tubal tissue and gene expression in PCOS is crucial for optimizing patient care and reducing the incidence of ectopic pregnancy. Future research should prioritize defining the precise pathways that connect therapeutic interventions to tubal alterations and implantation failure. This will facilitate the development of targeted treatments and improved risk stratification for this vulnerable population.