to be more genetically homogeneous than their associated clinical outcomes (Cannon & Keller, 2006), and so effects of individual genetic variants on endophenotypes are suspected to be larger and possibly easier to detect than the effect of those variants on the clinical outcome. Recent work suggests, however, that the effects of individual genetic variants on endophenotypes may not be appreciably larger than for complex and distal psychiatric or medical outcomes (Iacono et al. 2016). Using a community sample of over 4900 individuals from the Minnesota Twin Family Study (MTFS) (Iacono et al. 2014a), we have previously evaluated the genetic basis of 17 putative psychophysiological endophenotypes, including antisaccade eye movements, P300, electrodermal activity (EDA), resting electroencephalogram (EEG), and acoustic eyeblink startle, all of which were found to have moderate to high heritability and which, in past research, have demonstrated associations with various clinical outcomes, including schizophrenia. We conducted genome-wide association analyses (Malone et al. 2014a, b; Vaidyanathan et al. 2014a, b, c), analyses of array-based non-synonymous exonic variants (Vrieze et al. 2014b) and 11 whole genome sequencing (Vrieze et al. 2014c). Ultimately, we were neither able to convincingly corroborate any prior finding for any gene or variant previously associated with any
