Autism is a heterogeneous set of developmental disorders with complex etiologies. The goal of the symposium is to present a multidisciplinary perspective of how genetic, epigenetic, and environmental factors can interact to promote autism risk. The speakers will critically evaluate the evidence from human and animal studies that gene x environment interactions influence autism susceptibility, severity, and treatment outcomes. Genetic risk factors for autism will be reviewed. New evidence that autism may be associated with an increased copy number burden especially in regions of genomic instability, will be presented and discussed in relationship to environmental causes. How epigenetic mechanisms alter expression of genes relevant to autism will be reviewed in light of environmental chemicals that alter global and gene-specific DNA methylation patterns. Recent progress in understanding how impairments in neural connectivity contribute to autism will be reviewed. The role of methionine (MET) polymorphisms in autism risk and how polyaromatic hydrocarbons found in air pollution differentially influence individuals with the cMET autism risk allele will be presented. Evidence that low-level chemical exposures influence molecular and cellular processes that alter the balance of excitation and inhibition and neuronal connectivity relevant to the development of autism will be evaluated.