DVL2 (dishevelled segment polarity protein 2) is a key intracellular mediator of both canonical and non-canonical Wnt signaling pathways 1. DVL2 functions by binding to frizzled receptors and transducing Wnt signals to downstream effectors, particularly promoting β-catenin nuclear translocation through phosphorylation at serine 675 1. The protein undergoes extensive post-translational regulation, including phosphorylation by multiple kinases and dephosphorylation by phosphatases such as PP5 (PPP5C) 2. DVL2 stability is regulated through ubiquitination mechanisms, with WWP1-mediated K27-linked ubiquitination stabilizing the protein 3 and WWP2-mediated K63-linked ubiquitination promoting liquid-liquid phase separation critical for Wnt signaling 4. Clinically, DVL2 variants are associated with Robinow syndrome, a skeletal dysplasia disorder affecting WNT/planar cell polarity signaling 5. DVL2 polymorphisms have also been linked to increased risk of nonsyndromic cleft lip with or without cleft palate 6. The protein plays roles in cardiac hypertrophy through the DVL2/CaMKII/HDAC4/MEF2C pathway 3 and is involved in macrophage polarization via β-catenin signaling 7.