RABEP2 (rabaptin, RAB GTPase binding effector protein 2) is a critical regulator of vascular remodeling and ciliogenesis with significant implications for ischemic stroke outcomes. The protein plays a fundamental role in cerebral collateral circulation development, where genetic variants significantly impact stroke prognosis 1. Mechanistically, RABEP2 functions through endosomal trafficking pathways and interacts with SDCCAG8 at centrosomes to regulate ciliogenesis, which is essential for Hedgehog signaling 2. The protein serves as a substrate for GSK3 kinase, being phosphorylated at Ser200 and Ser204, though its precise cellular functions beyond Rab5 binding remain incompletely understood 3. Clinically, RABEP2 shows remarkable therapeutic potential in stroke treatment, as hypoxia-preconditioned bone marrow mesenchymal stem cells enhance collateral circulation through RABEP2 upregulation 4. Cross-species studies demonstrate that human RABEP2 coding variants predicted to be damaging result in decreased collateral vessel connections and increased cerebral infarct volume 5. The gene also shows genetic correlation with female body mass index and preeclampsia, suggesting broader roles in vascular dysfunction 6. These findings position RABEP2 as a promising target for personalized stroke therapy and risk stratification.