BEND5 (BEN domain containing 5) is a transcriptional repressor 1 that functions as a chr1 boundary factor and transcriptional modulator. BEND5 works synergistically with BEND4 to mark chr1 boundaries and promote early germ cell differentiation, particularly during epiblast-like cell (EpiLC) induction 2. Mechanistically, BEND5 suppresses transcription through its BEN domain, which directly interacts with the N-terminal domain of the transcription factor RBPJ/CSL 3. This interaction prevents the mastermind-like transcriptional coactivator (MAML) from forming a transcriptional activation complex with RBPJ, thereby inhibiting Notch signaling 3. In cancer biology, BEND5 acts as a tumor and metastasis suppressor. Low BEND5 expression correlates with advanced breast cancer stage and shortened overall survival 3. Functional studies demonstrate that BEND5 suppresses breast cancer cell growth and metastasis both in vitro and in vivo by inhibiting Notch signaling 3. Additionally, BEND5 expression is upregulated in arachnoid cyst membrane tissue compared to normal arachnoid membrane 4, suggesting potential involvement in membrane pathology. These findings position BEND5 as a promising therapeutic target for breast cancer treatment and identify BEND/Bend proteins as important regulators of gene expression during developmental and pathological processes.