The early 1990s marked a pivotal era in oncology with the elucidation of the molecular etiology of hereditary cancers, fundamentally transforming our understanding of genetic susceptibility. Ovarian cancer (OC) remains the most fatal gynecologic malignancy, often diagnosed at advanced stages with limited modifiable risk factors. Globally, it ranks as the eighth most frequently diagnosed cancer in women, underscoring its significant public health burden. Hereditary ovarian cancer (HOC), predominantly driven by pathogenic germline mutations in BRCA1 and BRCA2, confers a strikingly increased lifetime risk of OC. These tumor suppressor genes encode proteins essential for homologous recombination-mediated DNA repair, and their dysfunction promotes genomic instability. Risk assessment models, such as BRCAPRO and BOADICEA, facilitate early genetic screening, enabling the implementation of preventive strategies such as risk-reducing salpingo-oophorectomy (RRSO) and chemoprevention with oral contraceptives, both associated with reduced OC incidence. The advent of targeted therapies, particularly PARP inhibitors (olaparib, niraparib, and rucaparib), has revolutionized HOC management, exploiting synthetic lethality in homologous recombination-deficient tumors. These agents significantly improved progression-free survival, establishing them as a cornerstone of precision oncology. This review delineates the evolving landscape of HOC, focusing on pharmacoepidemiology, risk assessment, chemoprevention, and targeted therapy, aiming to refine clinical decision-making and advance precision medicine for improved patient outcomes.