Although recent studies have attributed the development of high-grade serous ovarian carcinoma with a p53 signature to the epithelial cells in distal fallopian tube [12, 13], induction of ovarian surface epithelial transformation was observed in several mouse models for ovarian tumors [14-17], and p53 mutations were also found in nonserous tumors such as high-grade endometrioid cancer [15, 16], suggesting potential involvement of the OSE cells and inclusion cysts in ovarian tumor development. This evidence concerns the gene TP53 and ovarian neoplasm.