Our group has been exploring the concept that developmental vitamin D (DVD) deficiency may be the plausible neurobiological explanation for several important epidemiological correlates of schizophrenia, namely 1) the excess winter/spring birth rate, 2) increased incidence of the disease in second-generation Afro-Caribbean migrants and 3) increased urban birth rate. We have produced two pieces of direct support for this hypothesis in patients. DVD deficiency therefore is a plausible ‘biological marker’ for schizophrenia. We have recently resolved a major technological barrier that will now allow us to test this hypothesis in a major European developmental biobank. The genetic factors or heritability indicators that would endow DVD deficiency as a valid schizophrenia endopheno-type are emerging. Our group has established a highly informative animal model to study the effects of DVD deficiency on brain development. This animal model reproduces the gross pathological features of the disease, that is, ventriculomegaly as well as sensitivity to amphetamine- and MK-801-induced hyperlocomotion and impairments in latent inhibition, behaviours analogous to the positive and negative symptoms of the disease in patients. We are now examining whether this model internally fulfils certain molecular endophenotypic criteria. Our initial data are encouraging as we find a 36 ± 11% decrease in the developmental expression of the candidate endophenotypic gene for schizophrenia, COMT. This animal model continues to provide good face and some construct validity with the disease in patients and illustrates how animal models can be used to progress plausible biological markers for schizophrenia into endophenotypes.