TUBGCP5 is a component of the gamma-tubulin ring complex (gTuRC) that mediates microtubule nucleation by regulating minus-end nucleation of alpha-beta tubulin heterodimers, a critical process for centrosome duplication and spindle formation 123. While primarily characterized for its role in microtubule organization, TUBGCP5 is clinically significant due to its involvement in neurodevelopmental disorders. Located in the chromosome 15.2 BP1-BP2 region, TUBGCP5 is one of four genes (with NIPA1, NIPA2, and CYFIP1) whose deletion causes Burnside-Butler syndrome, characterized by developmental delays, speech impairment, and behavioral problems 45. TUBGCP5 deletions are specifically associated with attention-deficit hyperactivity disorder (ADHD) and compulsions 6. The 15q11.2 microdeletion represents one of the most common pathogenic copy number variations in humans (0.6-1.3% prevalence), with larger Type I deletions (including TUBGCP5) producing more severe neurodevelopmental phenotypes compared to Type II deletions 5. Clinical manifestations in affected individuals range from asymptomatic to severe, including microcephaly, intellectual disability, seizures, and autism spectrum disorder, reflecting incomplete penetrance and variable expressivity 78.