In the last decade, psychiatric genetics has made tremendous progress in unraveling the genetic architectures of several highly heritable neurodevelopmental disorders, such as autism, attention deficit hyperactivity disorder (ADHD) and schizophrenia. However, it still remains to be understood, how polygenic risk emerges from multiple genetic lesion and how genetic risk impacts the brain during development to finally cause disease phenotypes. Translational research provides powerful tools to better understand the causal chain leading from genotypes to neural and behavioral phenotypes. Our panel will present different translational approaches, with special emphases being placed upon rare variants with high effect sizesand potential translational perspectives for clinical use. Andreas Reif will present behavioral findings in a mouse model with a conditional knock-out of the RBFOX1 gene, which has been linked to autism spectrum disorders. He will also introduce results from an imaging genetics study in human RBFOX1 carriers, which demonstrated altered neural reactivity to emotional stimuli in carriers. Thomas Nickl-Jockschat’s talk will focus on a mouse model of 16p11.2 deletion, a genetic strongly associated with autism and ADHD. This mouse model exhibits male-specific changes in reward-dependent behaviors and striatal circuits, the latter endophenotype seemingly shared by human carriers of that CNV. Andreas Meyer-Lindenberg will give an overview over neuroimaging phenotypes and potentially underlying molecular mechanisms in mouse models of three different CNVs. These mouse models suggest that microdeletions might increase risk for overlapping neuropsychiatric phenotypes through separable neural mechanisms. Finally, Franziska Degenhardt will present present exome sequencing findings in multiplex families with schizophrenia. She will also introduce first results from an outpatient clinic offering genetic testing for patients with neurodevelopmental disorders.