SLITRK2 is a postsynaptic transmembrane adhesion protein that functions primarily in excitatory synapse development and maintenance 1. The protein promotes excitatory synaptogenesis through interaction with presynaptic receptors, particularly receptor protein tyrosine phosphatases, via splicing-dependent trans-synaptic adhesion mechanisms 2. SLITRK2 negatively regulates TrkB (NTRK2) receptor levels in neurons 1. On dopaminergic neurons, SLITRK2 specifically promotes excitatory synaptic inputs while its family member Slitrk5 promotes inhibitory synapses; this balance is critical for normal locomotor activity 3. Functionally, SLITRK2 suppresses neurite outgrowth and regulates synapse organization 4. Clinically, SLITRK2 variants cause X-linked neurodevelopmental disorders characterized by intellectual disability, impaired spatial memory, and abnormal gait 1. Additionally, SLITRK2 variants modulate age-at-onset in C9orf72-associated frontotemporal dementia; higher SLITRK2 expression correlates with earlier disease onset and reduced synaptic vesicle proteins 5. Beyond neurodevelopment, elevated SLITRK2 expression associates with poor prognosis and advanced disease stage in gastric cancer, potentially through effects on immune cell infiltration 6.