EDAR (ectodysplasin A receptor) is a transmembrane receptor belonging to the TNF receptor superfamily that mediates critical signaling pathways essential for ectodermal organ development. EDAR specifically binds EDA isoform A1 (not A2) and signals predominantly through NF-κB and JNK pathways 1, with potential involvement in caspase-independent cell death. EDAR functions as a key component of the EDA/EDAR/NF-κB signaling cascade, which integrates with Wnt, Shh, and BMP pathways to regulate hair follicle morphogenesis, fingerprint ridge formation, and tooth development 23. During hair follicle development, EDAR signaling controls cell fate decisions in embryonic epidermis and regulates differentiation programs affecting hair initiation, shaft formation, and sebaceous gland morphology 1. Mutations in EDAR cause hypohidrotic ectodermal dysplasia (HED), characterized by defects in hair, teeth, and sweat glands 4. Additionally, an Asian-specific EDAR polymorphism (370V/A) influences tooth crown size and shoveling patterns, suggesting evolutionary selection 5. In pathological contexts, EDAR/NF-κB signaling contributes to psoriatic dermatitis through keratinocyte hyperproliferation and reduced apoptosis 6. EDAR thus represents a crucial developmental regulator with significant clinical relevance for ectodermal dysplasias and inflammatory skin diseases.