The fundamental premise of this essay, however, is that viewing relations among genes, behavior and the environment from the perspective of the classic diathesis–stress model of psychopathology, as so much psychiatric genetic research on G × E interaction does, may distort these relations and thereby undermine, rather than advance, the understanding of how genes and environment collectively operate to shape behavior and development, including risk of mental illness. Central to the diathesis–stress model is the postulate that some individuals are at heightened risk—because of their genetic make up—of succumbing to psychological disturbance when they encounter adversity, whereas others, lacking the genetic vulnerability, are not so affected even when exposed to the very same adversity. Thus, whereas an individual with a particular genetic vulnerability will be prone to develop a genetically specific disorder if he or she experiences what could be some particular or any of a variety of environmental stressors (for example, child abuse, negative life events, death of parent), the same environmental exposure will not engender psychopathology in an individual possessing a different version of the candidate gene in question.7
