By current standards in complex trait genetics, our study was small. Our hypothesis was that the size of genetic effects for endophenotypes would overcome the relatively small sample size. Clearly, genetic effects on these endophenotypes are not large enough to be detected in this sample. Given the cost of collecting laboratory-based psychophysiological endophenotypes like those used in the present research it appears that endophenotypes are less efficient for gene discovery than simply assessing and genotyping more cases and controls. However, it remains to be seen the extent to which endophenotypes can illuminate the mechanistic pathways between genes and clinical outcomes. While antisaccade and P300 are convincing putative endophenotypes in schizophrenia and EEG and electrodermal measures have also received significant support, multiple promising putative endophenotypes for schizophrenia were not available in the present research (Allen et al. 2009). Some of these endophenotypes may be associated with genetic loci of substantially larger effect sizes than any of our 17, although there is little evidence that psychophysiological or imaging-based endophenotypes are associated with larger effects than other complex traits and diseases (Iacono et
