DVL1 (dishevelled segment polarity protein 1) is a core signaling molecule that transduces Wnt signals from the cell membrane to downstream effectors, functioning in both canonical and non-canonical Wnt pathways 1. DVL1 binds to frizzled family receptors and requires nuclear localization to regulate cell proliferation in myoblasts 1. Additionally, DVL1 forms a ternary complex with PAK1 and MUSK to regulate acetylcholine receptor clustering during neuromuscular junction formation. DVL1 plays significant roles in multiple disease contexts. Mutations in DVL1 are associated with Robinow syndrome, an autosomal dominant skeletal dysplasia characterized by short limbs and facial anomalies, reflecting DVL1's importance in non-canonical Wnt-mediated skeletal morphogenesis 2. DVL1 is frequently overexpressed in prostate cancer (65% of cases), with expression levels correlating with tumor grade and progression through Wnt/Ξ²-catenin pathway activation 3. In hepatocellular carcinoma, DVL1 induction promotes Wnt pathway activation and ferroptosis resistance, marking it as a prognostic indicator of poor sorafenib response 4. DVL1 is also highly expressed in diabetes and has been identified as a potential molecular target 5, and shows elevated expression in retinoblastoma with positive correlations to N-myc 6. Clinically, DVL1 represents a therapeutic target for cancers dependent on aberrant Wnt signaling and potentially for metabolic diseases.