these alternative approaches such as the clustering strategy see (Drgon, et al., 2010)). The result of this approach has been a high degree of replication across studies. Table 2 presents an analysis from Uhl et al. (2008) which identified 50 genes that had been highly replicated in studies of drug dependence and related phenotypes. The p values in the table (from Uhl et al. (2008)) represent the probabilities of the repeated identification of these genes in so many studies based on Monte Carlo simulations. This list forms a stark contrast to the limited number of genes, of weak effect, generally identified in the linkage studies discussed above. With regard to the fact that each gene is not identified repeatedly in each study 100% of the time, it is important to note that 100 percent concordance should not be expected across studies for reasons mentioned above – that is, it is likely that the set of genes involved in drug dependence in different populations, in dependence on different substances, in different levels of dependence, and so forth, may not completely overlap. As this field progresses it is likely that we will be able to demonstrate different sets of genes associated with
