Autism spectrum disorder (ASD) comprises diverse neurodevelopmental trajectories in which altered circuit dynamics converge on a disturbance of excitation–inhibition balance. Genetic, postmortem, neuroimaging, and model-system evidence implicates γ-aminobutyric acid type A (GABAA) receptors as a major molecular node within this imbalance. ASD has been associated with changes in GABAA receptor subunit expression and assembly, notably within 15q11-q13 clusters, impaired receptor trafficking and sy