RHOJ is a plasma membrane-associated small GTPase belonging to the Cdc42 subfamily that functions as a molecular switch regulating cytoskeletal dynamics and cell migration 1. Its primary role involves angiogenesis, where it is specifically enriched in endothelial cells 2. RHOJ promotes endothelial cell migration during vascular development through direct interaction with glutamine synthetase (GLUL), which palmitoylates RHOJ to maintain its membrane localization and activation 3. Mechanistically, RHOJ elicits F-actin-rich structure formation by regulating actin cytoskeleton organization and can activate p21-activated kinase family members, influencing downstream effector activity 1. Beyond angiogenesis, RHOJ contributes to pathological processes including epithelial-to-mesenchymal transition in gastric cancer via IL-6/STAT3 signaling, promoting tumor invasion and metastasis 4. In pulmonary fibrosis, RHOJ marks a hyperglycolytic endothelial subset whose inhibition alleviates fibrosis and restores lung regeneration 5. Clinically, RHOJ overexpression correlates with poor cancer prognosis primarily through increased tumor angiogenesis and malignant cell phenotypes 1. These findings establish RHOJ as an emerging biomarker and therapeutic target for cancer and vascular diseases 1.