SLITRK3 is a transmembrane protein that suppresses neurite outgrowth and plays critical roles in synaptic development and neurological function. At the molecular level, SLITRK3 regulates inhibitory synapse assembly through trans-cellular interactions, particularly with ErbB4, facilitating postsynaptic specialization at GABAergic synapses 1. The protein is predominantly expressed in brain tissue with variable expression patterns across neural regions 2. Loss-of-function SLITRK3 variants cause epileptic encephalopathy characterized by seizures, intellectual disability, microcephaly, and developmental delay, with reduced parvalbumin-positive interneurons in knockout mice 3. SLITRK3 dysfunction impairs synaptic neurotransmission and peripheral/central nervous system development, positioning it as a key synaptic disease gene 3. Beyond neurological disorders, SLITRK3 shows dysregulation in various pathologies: upregulation in endometriosis-affected tissues 4, gastrointestinal stromal tumors where it predicts recurrence and metastasis 5, and triple-negative breast cancer as a tumor-infiltrating lymphocyte-related prognostic biomarker 6. SLITRK3 also associates with pain in Parkinson's disease through genetic variants affecting neurodevelopment 7, while reduced CSF levels correlate with unfavorable outcomes in VZV meningitis 8. These findings establish SLITRK3 as a multifunctional synaptic protein with broader implications in neuroinflammation and tumor biology.