Genome-wide association studies (GWAS) have identified thousands of single-nucleotide variants (SNVs) that are correlated with psychiatric disease risk. However, determining which among these are functionally relevant is a major challenge. Most are located in non-coding regions of the genome, and often it is unclear how they regulate gene expression and in which cell types and developmental periods this regulation is critical. In a recent paper in Nature Genetics, Guo et al. curated a list of 2,221 SNVs associated by GWAS with one or more of ten psychiatric disorders and used a massively parallel reporter assay approach to examine how disease-associated SNVs regulate gene expression relative to paired non-disease-associated SNVs in several human cell types. They identified 892 differentially active SNVs, which they mapped to specific genes, pathways, and cell types. Studies like this will hopefully help to illuminate how genetic variation contributes to brain disorders and identify new directions for treatments.