show Abstracthide AbstractPrenatal exposure to the histone deacetylase inhibitor VPA is known to increase risk for autism spectrum disorder (ASD) in children, and VPA-exposed rats exhibit a spectrum of autistic-like behaviors. However, it is unclear how VPA disrupts fetal brain gene expression in ways that may explain this increased risk. Here we examine how VPA dysregulates monkey fetal brain gene expression at birth in ways relevant to ASD-associated pathophysiology.