A major goal of the current analysis was to provide one example of how genetic information from GWAS and other approaches can be sorted based on potential function into a heuristic neurobiologic-functional framework (i.e., addiction cycle domains) that may enable improvements in prioritization of novel drug targets, improvements in the predictive value of genetic bio-markers and ultimately the integration of genomic information into a clinical diagnostic system. This approach is supported by the finding that the DSM-IV syndrome of alcohol dependence, and the current DSM-5 syndrome of AUD, do not reflect a single dimension of genetic liability, rather, dependence criteria from DSM-IV reflect at least three underlying dimensions that index genetic risk which is consistent with the genetic animal model literature (Kendler et al., 2012). This phenomenon is also seen for other common genetically complex psychiatric disorders such as depression (Kendler et al., 2013). These results underscore that the DSM disorders are primarily evolving theoretical constructs of unknown etiology rather than discrete neuro-pathologically defined diseases; while on the other hand, an accumulation of direct evidence supports an etiological basis of
