DVL3 (dishevelled segment polarity protein 3) is a core component of Wnt signaling pathways that functions as a membrane-associated protein propagating WNT signals from the cell membrane to the nucleus 1. DVL3 regulates multiple cellular processes including canonical and non-canonical Wnt/Ξ²-catenin signaling, planar cell polarity (PCP) pathways, and JNK cascade activation 2. Nuclear localization of DVL3 is essential for its function in regulating cell proliferation, requiring both its DIX and PDZ domains 1. Mechanistically, DVL3 activation occurs through frizzled receptor-mediated recruitment to the cell membrane, where it undergoes phosphorylation and activates downstream effectors including RAC1 and JNK signaling 2. Post-translational modification of DVL3 through PNPO-mediated oxidation promotes aberrant Wnt/Ξ²-catenin pathway activation 3. DVL3 dysregulation is implicated in multiple diseases. Robinow syndrome, autosomal dominant 3 results from DVL3 mutations. DVL3 overexpression promotes malignancy in multiple myeloma, non-small cell lung cancer, esophageal squamous cell carcinoma, and glioblastoma, correlating with advanced tumor stage and poor prognosis 3, 2, 4, 5. Additionally, decreased DVL3 expression associates with depressive disorder risk, with rs1969253 polymorphism conferring 3.3-fold increased depression susceptibility 6. In rheumatoid arthritis, exosomal DVL3 promotes fibroblast-like synovial cell aggression via Wnt pathway activation 7.