The findings of this study, if confirmed, call for expansion of research into the role of the AVP-OXT system variation in other social behaviors as mediators of DUD liability. Clearly, this variation is also potentially influenced by other genetic (as well epigenetic and nongenetic) mechanisms, some of which have already been detected. These include, for instance, the contribution of the MAOA gene and its interaction with parenting style to liability to DUD (61,62). It should be noted that even a nominally highly significant association finding may be difficult to replicate using purely genetic methods. Establishing mediation of a detected genetic association with the trait of interest (e.g., DUD risk) at a phenotypically intermediate level (e.g., gene expression; premorbid trait) would provide strong validity support, serving as both internal control and a mechanistic model test.
