In the case of schizophrenia, the overt symptom could be a psychosis, but the underlying phenotypes are, for example, a lack of sensory gating and a decline in working memory. Both of these traits have a clear genetic component and can thus be called endophenotypes. A strong candidate for schizophrenia endophenotype is prepulse inhibition, the ability to inhibit the reaction to startling stimuli. However, several other task-related candidate endophenotypes have been proposed for schizophrenia, and even resting measures extracted from EEG, such as, power of frequency bands and EEG microstates.
Endophenotypes are quantitative, trait-like deficits that are typically assessed by laboratory-based methods rather than by clinical observation.
The four primary criteria for an endophenotype are that it is present in probands with the disorder, that it is not state-related (that is, it does not occur only during clinical episodes) but instead is present early in the disease course and during periods of remission, that it is observed in unaffected family members at a higher rate than in the general population, and that it is heritable. The behavioral syndrome of schizophrenia is no longer thought to be a singular disease with a single underlying cause, as is once again becoming clear. Instead, it could have a number of different etiologies, and the symptoms could have many different origins. Such heterogeneity may explain some of the challenges in determining the genetics of schizophrenia and may also account for the clinical observations of schizophrenia treatment response variability. 
Some distinct genes that could underlie certain endophenotypic traits in schizophrenia include:
* RELN – coding the reelin protein downregulated in patients' brains. In one 2008 study, its variants were associated with performance in verbal and visual working memory tests in the nuclear families of patients.
* FABP7, coding the Fatty acid-binding protein 7 (brain), one SNP of which was associated with schizophrenia in one 2008 study, is also linked to prepulse inhibition in mice. It is still uncertain though whether the finding will be replicated for human patients.
* CHRNA7, coding the neuronal nicotinic acetylcholine receptor alpha7 subunit. alpha7-containing receptors are known to improve prepulse inhibition, pre-attentive and attentive states.