Endometriosis is a chronic, estrogen-dependent disorder marked by the presence of endometrial-like tissue outside the uterine cavity, which leads to symptoms such as pelvic pain and infertility. This review examines the role of hormonal regulation, particularly estrogen (E2) and progesterone (P4), in the disease's pathogenesis. The imbalance between E2 and P4 signaling is crucial, with elevated E2 levels promoting epithelial proliferation and P4 being vital for stromal decidualization. Disruptions in these hormonal pathways lead to P4 resistance and E2 dominance, which are key factors in endometriosis. The review focuses on genetic variations in hormone-related genes such as ESR1, ESR2, and PGR, and their effects on the disease. Significant alterations in gene expression have been observed, including upregulation of estrogen receptors and downregulation of progesterone receptors in endometriotic tissues. These changes suggest a dysregulated hormonal environment that drives disease progression by enhancing estrogen-driven growth and diminishing progesterone’s anti-inflammatory effects. Identifying these mechanisms is essential for developing targeted hormonal therapies and improving treatment strategies.