A new paradigm has been developed for the pathogenesis and origin of epithelial ovarian cancer (EOC), dividing it into two categories: type I and type II. Type I tumors, including low-grade serous, endometrioid, clear cell, and mucinous carcinomas, are generally indolent, confined to the ovary, and characterized by specific mutations such as KRAS, BRAF, CTNNB1, PTEN, PIK3CA, ARID1A, and PPR1A. They rarely harbor TP53 mutations and are genetically stable. Type II tumors, including high-grade serous, endometrioid, and carcinosarcomas, are aggressive, present in advanced stages, and have a high frequency of TP53 mutations. They also exhibit molecular alterations that disrupt BRCA function. Recent studies suggest that low-grade and high-grade serous carcinomas originate from fallopian tube epithelium rather than ovarian surface epithelium, and endometrioid and clear cell carcinomas arise from endometriosis. The origin of mucinous and Brenner tumors is still unclear, though recent data suggest they may originate from transitional epithelial nests near the tubo-peritoneal junction. This new paradigm indicates that both type I and type II tumors develop outside the ovary and involve it secondarily. This challenges the traditional view that EOC originates in the ovary. The paradigm has significant clinical implications, suggesting that prevention strategies such as salpingectomy with ovarian conservation may reduce the burden of ovarian cancer while preserving fertility and hormonal function. The identification of precursor lesions and the understanding of molecular pathways in EOC have led to new treatment approaches, including the use of PARP inhibitors for type II tumors. Prevention strategies are now being reevaluated, with a focus on reducing ovulation and avoiding unnecessary oophorectomies. The new paradigm emphasizes the importance of early detection, individualized treatment, and prevention, highlighting the need for further research to refine these approaches.A new paradigm has been developed for the pathogenesis and origin of epithelial ovarian cancer (EOC), dividing it into two categories: type I and type II. Type I tumors, including low-grade serous, endometrioid, clear cell, and mucinous carcinomas, are generally indolent, confined to the ovary, and characterized by specific mutations such as KRAS, BRAF, CTNNB1, PTEN, PIK3CA, ARID1A, and PPR1A. They rarely harbor TP53 mutations and are genetically stable. Type II tumors, including high-grade serous, endometrioid, and carcinosarcomas, are aggressive, present in advanced stages, and have a high frequency of TP53 mutations. They also exhibit molecular alterations that disrupt BRCA function. Recent studies suggest that low-grade and high-grade serous carcinomas originate from fallopian tube epithelium rather than ovarian surface epithelium, and endometrioid and clear cell carcinomas arise from endometriosis. The origin of mucinous and Brenner tumors is still unclear, though recent data suggest they may originate from transitional epithelial nests near the tubo-peritoneal junction. This new paradigm indicates that both type I and type II tumors develop outside the ovary and involve it secondarily. This challenges the traditional view that EOC originates in the ovary. The paradigm has significant clinical implications, suggesting that prevention strategies such as salpingectomy with ovarian conservation may reduce the burden of ovarian cancer while preserving fertility and hormonal function. The identification of precursor lesions and the understanding of molecular pathways in EOC have led to new treatment approaches, including the use of PARP inhibitors for type II tumors. Prevention strategies are now being reevaluated, with a focus on reducing ovulation and avoiding unnecessary oophorectomies. The new paradigm emphasizes the importance of early detection, individualized treatment, and prevention, highlighting the need for further research to refine these approaches.