Ovarian hyperstimulation syndrome (OHSS) is a severe complication of ovulation induction, particularly in the context of assisted reproductive technologies (ART). The syndrome’s pathophysiology centres on increased vascular permeability due to hormonal, vascular, and genetic factors, with human chorionic gonadotropin (hCG) as a key trigger. Recent insights underscore the role of vascular endothelial growth factor (VEGF), cytokines, and the renin-angiotensin-aldosterone system in OHSS. Genetic predispositions, including polymorphisms in FSH receptor genes and SNPs in pathways regulating ovarian and vascular function, further elucidate its pathogenesis. Clinically, OHSS presents a spectrum of severity, from mild discomfort to life-threatening complications such as thrombosis and organ failure. Classification systems, incorporating clinical symptoms and biomarkers like thrombin-antithrombin complex and VEGF levels, enhance diagnostic precision. Preventive strategies, including tailored stimulation protocols and alternative ovulation triggers like GnRH agonists, have reduced the incidence of severe OHSS. Advances in molecular research highlight the contributions of exosomal miRNAs, lncRNAs, and melatonin in modulating ovarian and vascular responses. Patient-specific factors, such as polycystic ovary syndrome and elevated oestradiol levels, also predict susceptibility. However, challenges persist in standardising diagnostic criteria and refining predictive tools. This chapter emphasises the importance of integrating genetic, clinical, and molecular insights into personalised prevention and management strategies. Future research should focus on refining classification systems, exploring novel biomarkers, and validating interventions through large-scale clinical trials to mitigate OHSS risks while optimising ART outcomes.