Variants associated with schizophrenia are thought to mediate disease risk by regulating chromatin accessibility and then gene expression. By integrating genome-wide SNP genotyping data with RNA-seq from 981 individuals, researchers can identify eQTL’s. By integrating SNP genotyping data with ATAC-seq data, researchers can identify chromatin accessibility QTL’s (caQTL’s). These eQTL/caQTL results can then be integrated with summary statistics from genome-wide association studies (GWAS) of schizophrenia or other neuropsychiatric diseases to identify genes, or ATAC-seq peaks than mediate disease risk54–56.
