arise due to shared disruptions of the mechanisms through which Val158Met genotype normally influences cortical development during childhood and adolescence. Because these disruptions are evident in both probands and unaffected relatives, they likely reflect shared genetic and/or environmental risk factors for schizophrenia, rather than secondary consequences of either active illness or its treatment. However, it is also possible that shared disruptions in COS probands and SIBs could reflect shared exposures that do not directly reflect risk factors for psychosis (e.g. changes in rearing environment due to parental responses to caring for a child with severe neurodevelopmental difficulties).
