To explore the mechanisms underlying ARID1B-related neurodevelopmental and psychiatric disorders, we generated Arid1b-haploinsufficient mice carrying a protein-truncating mutation at the start of exon 5 encoding the atrophin-1 domain of the protein and analyzed the resulting Arid1b+/– mice using transcriptomic, electrophysiological, and behavioral approaches (Fig. 1a–c; Supplementary Fig. 1a–c). This evidence concerns the gene ATN1 and psychiatric disorder.