We can summarize our argument with two points. The first is that there is little evidence that the observed variation in genetic architecture for intermediate phenotypes currently available is any different to that of other complex traits. The second is that, despite this, the limited understanding of the origins of psychiatric disease makes the acquisition of intermediate phenotypes that capture the mechanisms underlying disease processes essential to the interpretation genetic findings. This process is conceptually no different from the acquisition of physiological information to interpret a molecular explanation of disease origin. In particular, the use of the term endophenotype obfuscates the traditional process of understanding pathogenesis by casting undue weight on the genetic component of the measure and by assuming that the phenotype is part of the causal pathway from genetic variant to disease [13]. We may be better served by working to improve the precision of our phenotypes, and thereby reduce measurement error (see Box 2).
