CNTNAP4 (contactin-associated protein-like 4) is a presynaptic transmembrane protein belonging to the neurexin superfamily that plays critical roles in neurotransmitter regulation and neural development 1. The protein functions as a key regulator of both dopaminergic and GABAergic synaptic transmission, with deficiency leading to decreased GABA release and increased dopamine release 2. Mechanistically, CNTNAP4 regulates GABAergic signaling through interactions with GABAA receptor β2/3 subunits and GABAA receptor-associated protein (GABARAP), influencing receptor membrane localization without affecting total protein levels 3. The protein also serves as a receptor for neural EGFL-like 1 (Nell-1), mediating osteogenic signaling through Wnt and MAPK pathways 2. CNTNAP4 deficiency is clinically significant across multiple disorders. In Parkinson's disease, reduced CNTNAP4 expression in dopaminergic neurons induces α-synuclein pathology, neurodegeneration, and motor dysfunction through disrupted mitophagy and increased neuroinflammation via astrocyte-microglia C3-C3aR signaling 41. The gene is also implicated in autism spectrum disorders, with knockout mice displaying repetitive behaviors and altered brain-testicular gene expression affecting mitochondrial function and synaptic signaling 5. Additionally, CNTNAP4 expression changes are associated with epilepsy susceptibility and osteosarcoma progression, highlighting its broad pathological relevance 36.