The use of a combined systems biology and GEM approach will ideally account for more genetic variance in a particular phenotype than that which can be attributed to any single genetic variant. In some cases, this may complicate the clinical translation of these findings as single variant findings are more readily translatable into pharmacologically-based interventions whereas the likely group of variants implicated by a systems biology approach may span multiple neurotransmitter systems in a fashion not readily amenable to monotherapies or medication development. Systems biology may highlight a particular biological pathway that could be targeted pharmacologically at various levels (e.g., presynaptically, synaptically or postsynaptically). However, this information offers a distinct advantage over single variant methods by providing an increased understanding of epistasis, or interactions of genes relevant to potentially different neurotransmitter systems. Accordingly, it is possible that these systems based approaches may define the genetic contributions to larger scale polygenic phenomena that could be targeted behaviorally. For example if variation in multiple genes were implicated in explaining differential urge for alcohol (in a fashion that was not readily addressed through
