GLDN (gliomedin) is a cell surface ligand that mediates axon-glial cell interactions essential for nervous system development and function. It serves as a ligand for NRCAM and NFASC/neurofascin, facilitating interaction between Schwann cell microvilli and axons [UniProt]. GLDN is required for normal clustering of sodium channels at heminodes during node of Ranvier formation and, together with NRCAM, maintains NFASC and sodium channel clusters at mature nodes—structures critical for saltatory propagation of action potentials [UniProt]. Pathogenic recessive variants in GLDN cause lethal congenital contracture syndrome 11 (LCCS11), clinically presenting as arthrogryposis multiplex congenita (AMC) with congenital joint contractures 1. GLDN-associated AMC is now recognized as a viable condition with significant neonatal support, classified as a fetal akinesia deformation sequence 2. Functional studies confirm pathogenicity of novel variants including p.Leu365Phe and previously reported variants 2. Beyond neuromuscular function, GLDN+ cells represent a previously uncharacterized population of odontogenic stem cells essential for dental pulp development and regeneration, functioning through BMP5 signaling mechanisms 3. GLDN expression is downregulated in gastric intestinal metaplasia, serving as a potential biomarker 4. GLDN+ stromal cell subsets have been identified in human lymph nodes with specialized immunomodulatory functions 5.