Through technological innovations and international collaboration, we are finally succeeding in identifying some of the common and rare genetic loci that affect risk for psychiatric disorders. The first successful studies told us that samples sizes need to be maximized and no parts of the genome should be left out of investigation. While we are working to meet these requirements to find more of the underlying risk factors, our increasing knowledge about the genetic architecture of brain disorders can also help us to improve gene-finding. Potentially the most promising of those is the apparent existence of a genetic continuum stretching from psychiatry-related traits in the general population to specific psychiatric disorders and severe intellectual disability. I will show examples on how such knowledge can speed up the identification of genes for different psychiatric disorders.Having found ways to eliminate bottlenecks in gene-finding, our field is running into new ones where we are trying to understand, how the identified risk factors contribute to disease risk. For the mapping of the biological pathways from gene to a psychiatric disorder, complementary methods at different levels of organismal complexity are needed. This requires interdisciplinary approaches, most efficiently achieved through collaboration. Much about molecular processes implicated by the disorder-associated genes can be retrieved from existing information through bioinformatics. In addition, cell-based models and animal models, in which we can perform targeted gene-manipulation, are highly effective for testing hypotheses. These models lend themselves also to unravel effects of risk genes at the cellular level. Importantly, the current high speed of gene discovery should be taken into account when setting up such models, as fast and inexpensive ones are to be preferred. In my lab, we have chosen to work with induced neurons based on human induced pluripotent stem cell technology and with an animal model based on Drosophila melanogaster. For the latter, we have been able to show several ADHD genes to increase activity in the fly, and have confirmed the involvement of dopaminergic and circadian signaling routes in ADHD-like symptoms. Finally, to understand effects of risk genes on the human brain in vivo, we employ neuroimaging genetics designs. This field of research has suffered in the past from uncountable reports of underpowered, single variant studies of brain regions of interest, which people have not been able to replicate. However, through international collaboration, very large sample sizes have been collected through e.g. the ENIGMA Consortium, which provide the basis for highly powered studies investigating the overlap between disease genes and genes for brain phenotypes. In this way, we were recently able to show ADHD risk loci to influence intracranial volume.A thorough understanding of the biological basis of psychiatric disorders seems indispensable, if we aim at improving the life quality of patients by providing better diagnostic services and develop novel treatment options for the future.