SATB2 is associated with schizophrenia and is an important transcription factor 
regulating neocortical organization and circuitry. Rare mutations in SATB2 cause 
a syndrome that includes developmental delay, and mouse studies identify an 
important role for SATB2 in learning and memory. Interacting partners BCL11B and 
GATAD2A are also schizophrenia risk genes indicating that other genes 
interacting with or are regulated by SATB2 are making a contribution to 
schizophrenia and cognition. We used data from Satb2 mouse models to generate 
three gene-sets that contain genes either functionally related to SATB2 or 
targeted by SATB2 at different stages of development. Each was tested for 
enrichment using the largest available genome-wide association studies (GWAS) 
datasets for schizophrenia and educational attainment (EA) and enrichment 
analysis was also performed for schizophrenia and other neurodevelopmental 
disorders using data from rare variant sequencing studies. These SATB2 gene-sets 
were enriched for genes containing common variants associated with schizophrenia 
and EA, and were enriched for genes containing rare variants reported in studies 
of schizophrenia, autism and intellectual disability. In the developing cortex, 
genes targeted by SATB2 based on ChIP-seq data, and functionally affected when 
SATB2 is not expressed based on differential expression analysis using RNA-seq 
data, show strong enrichment for genes associated with EA. For genes expressed 
in the hippocampus or at the synapse, those targeted by SATB2 are more strongly 
enriched for genes associated EA than gene-sets not targeted by SATB2. This 
study demonstrates that single gene findings from GWAS can provide important 
insights to pathobiological processes. In this case we find evidence that genes 
influenced by SATB2 and involved in synaptic transmission, axon guidance and 
formation of the corpus callosum are contributing to schizophrenia and 
cognition.