DIP2B (Disco-interacting protein 2 homolog B) is a conserved protein with multiple cellular roles. Functionally, DIP2B negatively regulates axonal outgrowth and is essential for normal synaptic transmission [UniProt], promoting acetylation of alpha-tubulin. The gene contains functional domains including an Acyl-CoA synthetase domain and AMP-binding sites, linking it to metabolic regulation 1. DIP2B dysfunction has significant clinical relevance across multiple disease contexts. Loss-of-function variants in the paralog DIP2C are associated with expressive speech delay and developmental delays 1, suggesting DIP2B may have comparable neurodevelopmental functions. CGG trinucleotide repeat expansions in DIP2B contribute to neurodevelopmental disorders through epigenetic silencing 2, and expanded tandem repeats near DIP2B promoters cause gene silencing through DNA hypermethylation in cardiomyopathy 3. Notably, DIP2B tandem repeat expansions account for approximately 4% of cardiomyopathy risk. In cancer, DIP2B exhibits context-dependent roles. It acts as a tumor suppressor in renal cell carcinoma, where elevated expression correlates with improved survival 4, but shows oncogenic properties in breast cancer and lung adenocarcinoma, where high expression predicts poor prognosis and associates with reduced immune cell infiltration 5. Genetic variants affecting DIP2B alternative polyadenylation influence cancer susceptibility across multiple cancer types 6. Gene fusions involving DIP2B (DIP2B::BRAF) have been identified in melanomas 7.