The utility of our 17 endophenotypes for characterizing genetic effects on neurobehavioral mechanisms in clinical samples remains to be seen, and is currently being pursued through work such as that being done by the Consortium on the Genetics of Schizophrenia (COGS). COGS is also evaluating a greater number of putative endophenotypes for study. COGS uses clinical probands to recruit families, thus increasing the variance of endophenotype expression in their sample and ensuring high levels of genetic risk in the unaffected individuals. They have reported on multiple heritable endophenotypes that differentiate cases and controls but it is currently unclear the extent to which they have discovered individual genetic loci robustly associated with any of their schizophrenia-related endophenotypes after one employs standard multiple testing and ancestry corrections (Greenwood et al. 2011, 2016). Case–control samples like COGS and the PGC, because they employ an extreme sampling design, are more powerful than community samples for investigations of genetic association with disorders like schizophrenia. However, when the goal is to test known schizophrenia genetic loci for association with known schizophrenia-relevant endophenotypes, a case–control study of
