When performing TWAS using Edu Attainment GWAS (imperfect proxy for cognitive ability) on gene expression during VPA exposure, many significantly associated genes were identified, which were enriched in folate metabolism.

Many common genetic variants impacted chromatin accessibility or gene expression in this population (black circles are significant interaction molQTLs). Showing that inherent genetic variation does impact response to drugs.

VPA also strongly shuts down proliferation, measured through an EdU assay, consistent with prenatal VPA exposure leading to microcephaly.

Genes differentially expressed due to VPA replicated previous work and were enriched in genes associated with autism through whole exome sequencing, again suggesting convergence.

We found GWAS heritability for ASD and intelligence was strongly enriched within peaks differentially accessible due to VPA exposure, suggesting a convergence of genetic and environmental factors.

We added VPA, an anticonvulsant and mood stabilizer where prenatal exposure is associated with intellectual disability and autism, as well as Li, used for treatment of bipolar disorder, to a population of genotyped human neural progenitors.