Failure to replicate direct effects of candidate vulnerability genes on specific psychopathological conditions suggests that genes may not influence behavior directly, leading many investigators to examine how genes may moderate effects of the environment on human G × E interaction. One well-studied G × E interaction involves monoamine oxidase-A (MAOA), contextual adversity and antisocial behavior. The interaction of a functional MAOA gene polymorphism (MAOA-uVNTR) and childhood adversity, first detected by Caspi et al.2 in their research on child maltreatment, has now been replicated enough times that meta-analysis reveals it to be reliable3—despite claims by some to the contrary.4 Thus, there is growing evidence that individuals possessing the low-MAOA-activity allele are predisposed to become antisocial when they experience a variety of adverse experiences, most notably maltreatment in childhood.
