NLGN2 is a transmembrane cell-adhesion molecule that serves as a central organizer of inhibitory GABAergic synapses 1. It functions exclusively at inhibitory synapses, unlike its paralog NLGN1 which operates at excitatory synapses, with this specificity determined by extracellular domains 2. NLGN2 recruits and clusters postsynaptic proteins including GABRG2 and gephyrin through transsynaptic interactions with presynaptic neurexins, thereby regulating signal amplitude from inhibitory synapses and modulating the excitatory/inhibitory balance critical for information processing 1. It also promotes initial synapse formation and may facilitate de novo presynaptic structure development. Beyond neurons, NLGN2 mediates cell-cell interactions in pancreatic beta cells and modulates insulin secretion. Dysregulation of NLGN2 is implicated in multiple neurodevelopmental and psychiatric disorders. Rare mutations including R215H cause loss-of-function deficits in GABAergic synaptogenesis through endoplasmic reticulum retention and impaired membrane trafficking in schizophrenia 3. NLGN2 was identified as a high-confidence neurodevelopmental disorder candidate gene 4 and a potential therapeutic target for migraine 5. Its altered expression in the prefrontal cortex associates with memory consolidation processes 6, and structural variants implicate NLGN2 in autism spectrum disorders 7.