ELMO2 is a cytoskeletal adaptor protein essential for cell migration and apoptotic cell engulfment. Functionally, ELMO2 acts as a scaffolding component that associates with DOCK1, ILK, and RhoG to regulate Rac1 activation 1, a small GTPase critical for cytoskeletal rearrangement and lamellipodia formation 2. In phagocytosis, ELMO2 participates in a novel ILK/RhoG/ELMO2 pathway that mediates Rac1-dependent uptake of apoptotic cells; knockdown of ELMO2 reduces phagocytosis by approximately 51% 3. ELMO2 also integrates receptor tyrosine kinase signaling: Axl phosphorylates ELMO2 on Tyr-713 to promote Rac1 activation and cancer cell invasion 4, while HGF-induced MET-AXL complex formation recruits ELMO2-DOCK180 to enhance migration 5. Mechanistically, ELMO2 regulates vascular smooth muscle cell adhesion and contractility through Rac1-dependent actin dynamics 6. Disease-wise, loss-of-function ELMO2 mutations cause primary intraosseous vascular malformation (VMOS) with craniofacial bone expansion and vascular anomalies, including aneurysms in the carotid artery 6, overlapping with Ramon syndrome characterized by cherubism and gingival hypertrophy 7. These findings establish ELMO2 as a central coordinator of cell migration, cytoskeletal dynamics, and vascular development.