NOG encodes noggin, a secreted polypeptide that functions as an inhibitor of bone morphogenetic proteins (BMP) signaling, which is essential for growth and patterning during human development, particularly in cartilage and bone formation 1. The protein plays a critical role in regulating multiple signaling pathways, with its hallmark clinical feature being proximal symphalangism, characterized by abnormal fusion of the proximal interphalangeal joints of the hands and feet 1. Mechanistically, noggin inhibits chondrocyte differentiation through interactions with growth differentiation factors and negatively regulates SMAD protein signaling pathways. Mutations in NOG cause a spectrum of autosomal dominant syndromes including proximal symphalangism, multiple synostoses syndrome 1, stapes ankylosis with broad thumbs and toes, tarsal-carpal coalition syndrome, and brachydactyly type B2 1. Clinical variants such as 672 C/A and 567 G/C have been associated with mandibular micrognathism 2. The overlapping phenotypic spectrum of NOG-related disorders has led to the proposed unifying term 'NOG-related symphalangism spectrum disorder (NOG-SSD)' for improved clinical recognition 1. Additionally, Myo/Nog cells expressing noggin have been identified in retinal tissues where they provide neuroprotective effects against hypoxia-induced cell death 3.