Glass syndrome, also known as SATB2-associated syndrome, is a rare neurodevelopmental disorder caused by variants or deletions involving the SATB2 gene on chromosome 2q33.1. The condition is characterized by intellectual disability, growth and mental retardation, microcephaly, epilepsy, and distinctive craniofacial features such as micrognathia (small jaw), down-slanting palpebral fissures, cleft palate, crowded teeth, and sometimes microglossia (small tongue) and thyroid anomalies. Glass syndrome follows an autosomal dominant inheritance pattern, with most cases resulting from de novo (new) mutations rather than inherited changes. The age of onset is typically in early childhood, often recognized due to developmental delays and congenital anomalies. The syndrome shows considerable phenotypic variability, with some individuals experiencing more severe craniofacial or functional issues than others. Penetrance appears to be high, as most individuals with pathogenic SATB2 variants display clinical features, though the severity and specific symptoms can vary. Population frequency is very low, making it an ultra-rare disorder.