Analyses of model organisms provide the relevant information. We will discuss two examples. The first is genetic analysis of phenotypes in the mouse, from which we have robust genome-wide association data for multiple phenotypes, behavioural and physiological, and associated estimates of locus effect sizes. These data allow us to compare the genetic architecture of behavioural phenotypes with those that would qualify as endophenotypes: for instance measures of electrophysiology, biochemistry, haematology and immunology. The drawback is that mouse models of psychiatric disease are imperfect, so that inferences drawn from the mouse data may be misleading. Nevertheless, we have no reason to expect the relationship between endophenotypes and behavioural phenotypes to be different in rodents and humans.
