However, as noted above, it is important to note that, while the analytic approach that we use here seeks to identify genes with variants that are likely to play roles in addiction and in related phenotypes, there are limitations to interpretation of this data that come from our belief that flexible approaches to identification of such genes are likely to benefit analyses such as those that are presented here. If we allow for locus heterogeneity, for sample-to-sample differences in the details (including the phase) of linkage disequilibrium between marker alleles and pathogenic alleles, and for the use of different marker sets with different datasets, then we cannot demand that all samples display the more stringent criterion: significant association of the same SNP with the same phase in all samples. This approach thus seeks to use stepwise analyses to identify and confirm statistically-significant association at the level of individual gene loci, assuming that subsequent followup analyses will use further steps to untangle any locus heterogeneity, to unequivocally identify which individual SNPs are associated, to identify pathological haplotypes and the phases with
