FOXL2 is a key transcription factor in ovarian development and maintenance throughout life. Despite advanced knowledge about its role, its transcriptional regulation in the ovary is poorly understood. Most of the insights into FOXL2 regulation come from non-coding genetic defects we found in blepharophimosis syndrome (BPES), a rare, autosomal dominant syndromic form of primary ovarian insufficiency (POI), and from a goat and mouse model. We aim to answer outstanding key questions on the 3D topology and regulatory landscape of the FOXL2 region in human ovarian granulosa cells (GCs) using C-technologies and multi-omics, and to understand the impact of non-coding defects of the FOXL2 region on 3D topology and molecular pathways in BPES disease models. Key objectives are: (1) To map the 3D genome topology and regulatory landscapes in human GCs using C-technologies and multi-omics; (2) To functionally validate ovarian cCREs and lncRNAs of the FOXL2 region; (3) To determine the impact of non-coding deletions of the FOXL2 region on 3D topology and expression in BPES disease models. Overall, this work will advance genomic studies of more frequent ovarian diseases such as POI, occurring in 1% of the female population.