assay noise. We thus identify more chromosomal regions and genes based on the overlap between the chromosomal regions identified by data from each sample than we would expect if the only reason for clustering of nominally positive SNPs in each sample was stochastic variation in the frequencies with which blocks of restricted haplotype diversity are found in cases vs controls that are unrelated to the phenotype. Availability of data from other recently-reported genome wide association studies also provides a third way in which we seek replication, based on identification by the current data, of more of the same genes that were identified in other reports from independent samples and different analyses than we would expect by chance. This comparison also provides additional means for us to refute then null hypothesis that the clustering observed in each sample derives from stochastic case vs control differences in haplotype frequencies rather than case vs control differences that are truly related to differences in phenotypes. In replicated samples that compared 500 k allele frequencies in alcohol dependent to population control samples, Treutlein and colleagues [15] have used a mixed analytic strategy to identify nine genes. Products of two of these genes, ADH1C and PECR,
