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Thrombophilia, characterized by a heightened propensity for blood clotting, is a significant contributor to RSA. This review examines the mechanisms connecting thrombosis and RSA, focusing on hypercoagulable states, placental thrombosis, inflammation, and endothelial dysfunction. Genetic and acquired thrombophilic factors, such as factor V Leiden mutation, prothrombin gene mutation, protein C and S deficiencies, antithrombin III deficiency, antiphospholipid syndrome, and hyperhomocysteinemia, are discussed in detail. The diagnosis of thrombophilia in RSA entails a comprehensive clinical evaluation, including the assessment of physical examination, medical history and laboratory investigations, although there is still debate over the need for universal screening. Therapeutic strategies, including anticoagulant and antiplatelet therapies, as well as lifestyle modifications, are tailored to individual risk factors and disease severity. 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