RASD2 is a GTPase signaling protein that binds and hydrolyzes GTP, functioning as a key regulator of G-protein-coupled receptor signaling pathways 1. It modulates heterotrimeric G-protein interactions and promotes SUMOylation of downstream targets 2. The protein is enriched in striatal tissue where it modulates dopaminergic neurotransmission and influences motor coordination and locomotor activity 1. Mechanistically, RASD2 regulates multiple cellular processes including glycolysis enhancement through HK2, LDHA, GLUT1, and PKM2 expression 3, and SUMOylation-mediated protein stabilization 2. In the striatum and prefrontal cortex, RASD2 interacts with β-arrestin2 to modulate dopamine receptor signaling 4. Disease relevance spans psychiatric and oncologic conditions. Genetic variations in RASD2 associate with schizophrenia-related prefrontal and striatal phenotypes, with reduced expression observed in schizophrenia patients 14. RASD2 is significantly upregulated in uveal melanoma 3, thyroid cancer 5, and endometriosis 2, where elevated expression correlates with poor prognosis and enhanced metastatic potential. RASD2 overexpression promotes tumor cell proliferation, invasion, and glycolytic metabolism. Clinically, RASD2 represents a therapeutic target; miRNA-485-5p and miRNA-4763-3p negatively regulate RASD2 54, and inhibiting RASD2 suppresses tumor growth and metastasis in vivo 35. RASD2 also serves as a potential schizophrenia biomarker 4.