Background/Aim: We describe a rare case of ovarian mesonephric-like adenocarcinoma (MLA) involving the fimbria and mimicking serous tubal intraepithelial carcinoma (STIC). Case Report: A 47-year-old woman presented with a 4.4-cm left ovarian mass. Histologically, the ovarian tumor showed papillary and solid architecture, severe nuclear pleomorphism, and increased mitotic activity. Some microscopic foci where the tumor cells spread horizontally along the fimbrial surface epithelium were noted, compatible with STIC. We initially considered the ovarian tumor to be high-grade serous carcinoma accompanied by a fimbrial STIC. However, immunostaining revealed nuclear immunoreactivity for paired box 2 and GATA-binding protein 3, but lacked expression of Wilms tumor 1. A thorough slide review and additional immunostaining revealed architectural diversity, densely eosinophilic intraluminal secretions, and lack of hormone receptor expression, supporting the diagnosis of MLA. Conclusion: Microscopic intraepithelial metastases of the MLA to the fimbria mimic STIC. We recommend ancillary tests, such as immunostaining, in patients with ovarian tumors whenever possible, particularly for those with differential diagnosis of MLA and high-grade serous carcinoma.Ovarian carcinoma is the deadliest gynecological malignancy, accounting for more than 14,000 deaths each year (1). Highgrade serous carcinoma (HGSC) is the most prevalent and aggressive subtype of ovarian carcinoma, accounting for 70% of ovarian carcinoma-related deaths. The fallopian tube has recently emerged as an important site of origin not only for tubo-ovarian HGSC in patients with germline mutation of breast cancer 1 (BRCA1) or BRCA2, but also as a source of peritoneal HGSC (2). A thorough histological examination of resected ovaries and fallopian tubes has led researchers to focus on investigating the carcinogenesis of tubo-ovarian HGSC from the fallopian tube. Increasing evidence suggests that the distal part of the fallopian tube, particularly the fimbria, is the origin of tubo-ovarian and peritoneal HGSCs, and serous tubal intraepithelial carcinoma (STIC) is the precursor lesion (3). STIC is morphologically characterized by the proliferation of non-ciliated epithelium, showing stratification, loss of polarity, severe nuclear pleomorphism, conspicuous nucleoli, and increased mitotic activity (1, 4). In addition to these histological criteria, more than 90% of STICs harbor mutations of tumor protein 53 (TP53), resulting in aberrant expression of p53 on immunostaining. Therefore, the lesions typically demonstrate either p53 overexpression (indicating missense mutations) or complete absence of p53 staining (indicating nonsense or frameshift mutations) (5).