AIDA (axin interactor, dorsalization associated) encodes the AIDA-1 protein, which plays critical roles in neurodevelopment and synaptic function. AIDA-1 is a brain-specific protein highly enriched at neuronal synapses that regulates synaptic plasticity 1. The protein functions as a ventralizing factor during embryogenesis by inhibiting axin-mediated JNK activation through binding axin and disrupting axin homodimerization, thereby antagonizing Wnt/β-catenin-independent dorsalization pathways. Beyond its developmental role, AIDA-1 has significant clinical relevance in neurodevelopmental disorders. Heterozygous microdeletions in ANKS1B (encoding AIDA-1) cause ANKS1B haploinsufficiency syndrome (ANDS), characterized by autism spectrum disorder, attention-deficit hyperactivity disorder, and speech and motor deficits 1. Importantly, AIDA-1 also regulates oligodendrocyte function and myelination, with selective loss from oligodendrocytes leading to social behavior deficits 2. Mouse models of Anks1b haploinsufficiency recapitulate patient phenotypes including social deficits, hyperactivity, and sensorimotor dysfunction 1. The AIDA-1 interactome reveals protein networks involved in synaptic function and neurodevelopmental disorder etiology, establishing AIDA-1 as a key regulator of both neuronal and oligodendroglial functions critical for proper brain development and social behaviors.