GLRB encodes the β-subunit of heteromeric glycine-gated chloride channels 1, forming the predominant glycine receptor (GlyR) population in postnatal and adult brain, brainstem, and spinal cord 1. These 2α1:3β pentameric channels mediate inhibitory neurotransmission by generating glycine-activated chloride currents that suppress neuronal excitability 1. GLRB plays a critical role in downregulating neuronal excitability and contributing to inhibitory postsynaptic current generation 2. Pathologically, GLRB mutations are the third major genetic cause of hyperekplexia, a neonatal/pediatric startle disorder characterized by excessive startle reflexes, hypertonia, and generalized stiffness 1. Recessive null mutations (nonsense, frameshifts, large deletions) and dominant missense variants cause severe phenotypes including apnea attacks, learning difficulties, and developmental delay 1. Additionally, non-coding GLRB polymorphisms (rs78726293, rs191260602, rs17035816, rs7688285) are associated with panic disorder and agoraphobia through increased startle response and fear network activation 3. Partial Glrb knockout mice exhibit agoraphobic phenotypes, supporting a mechanistic link between GLRB dysfunction and anxiety disorders 3. These variants regulate GLRB and nearby gene expression in brain tissues 4, providing a potential neurogenetic pathway linking glycinergic signaling deficits to psychiatric disease.