Stefansson and his team have used the breadth of the company's datasets and links between diseases and traits to discover new risk variants for mental illness, but also to refine the understanding of the perturbations that define these conditions and the nature of cognition itself. Studies in the early 2000s mapped the involvement of the Neuregulin 1 gene in schizophrenia, leading to substantial research in this novel pathway.  Over the next fifteen years they used standard GWAS and reduced fecundity as an intermediate phenotype to home in on SNPs and copy number variations (CNVs) linked to risk of schizophrenia and other disorders;  they demonstrated that genetic risk factors for schizophrenia and autism confer cognitive abnormalities even in control subjects;  they linked schizophrenia, bipolar disorder with both creativity and risk of addiction;  they identified genetic variants associated with educational attainment and childhood cognition; and demonstrated that these variants are currently under negative evolutionary selection.  In addressing common psychiatric disorders and cognitive processes and traits across a population, this body of work has contributed to the present understanding of these conditions not as discrete phenotypes but as related through the disruption of fundamental cognitive functions.