The article by Kurman and Shih presents a new paradigm for the pathogenesis and origin of epithelial ovarian cancer (EOC), based on recent morphologic, immunohistochemical, and molecular genetic studies. This paradigm divides EOC into two broad categories: Type I and Type II tumors. Type I tumors, including low-grade serous, low-grade endometrioid, clear cell, and mucinous carcinomas, are generally indolent, present in stage I, and characterized by specific mutations such as KRAS, BRAF, ERBB2, CTNNB1, PTEN, PIK3CA, ARID1A, and PPP1RA, but rarely TP53. These tumors are genetically stable. Type II tumors, including high-grade serous, high-grade endometrioid, malignant mixed mesodermal tumors, and undifferentiated carcinomas, are aggressive, present in advanced stages, and have a very high frequency of TP53 mutations but rarely harbor the mutations found in Type I tumors. They are also characterized by molecular alterations that affect BRCA expression. Recent studies suggest that fallopian tube epithelium and endometriosis are the precursors of these tumors, rather than the ovarian surface epithelium. This new paradigm has important clinical implications, suggesting that prevention approaches, such as salpingectomy with ovarian conservation, may play a significant role in reducing the burden of ovarian cancer while preserving hormonal function and fertility.The article by Kurman and Shih presents a new paradigm for the pathogenesis and origin of epithelial ovarian cancer (EOC), based on recent morphologic, immunohistochemical, and molecular genetic studies. This paradigm divides EOC into two broad categories: Type I and Type II tumors. Type I tumors, including low-grade serous, low-grade endometrioid, clear cell, and mucinous carcinomas, are generally indolent, present in stage I, and characterized by specific mutations such as KRAS, BRAF, ERBB2, CTNNB1, PTEN, PIK3CA, ARID1A, and PPP1RA, but rarely TP53. These tumors are genetically stable. Type II tumors, including high-grade serous, high-grade endometrioid, malignant mixed mesodermal tumors, and undifferentiated carcinomas, are aggressive, present in advanced stages, and have a very high frequency of TP53 mutations but rarely harbor the mutations found in Type I tumors. They are also characterized by molecular alterations that affect BRCA expression. Recent studies suggest that fallopian tube epithelium and endometriosis are the precursors of these tumors, rather than the ovarian surface epithelium. This new paradigm has important clinical implications, suggesting that prevention approaches, such as salpingectomy with ovarian conservation, may play a significant role in reducing the burden of ovarian cancer while preserving hormonal function and fertility.