Given the low power of genetic linkage analyses in general community samples, relative to finding genetic association (42), and the accumulating evidence for small effect sizes, our failure to find genomewide significant linkage signals is unsurprising. However, whereas findings for heaviness of drinking were uniformly negative (LOD scores <1.5), for AUD-FS our second highest peak coincided with a location identified in previous alcoholism linkage studies (Chr2, LOD 2.22 at 112cM (8,43)) while a second peak (Chr10, LOD 2.02 at 152cM) occurred within approximately 20cM of the peak reported in (44). We did not find evidence for clustering of SNP associations in these regions. In association analyses, while in a few cases we found suggestive convergence for consumption versus dependence phenotypes, or between inferences from family-based versus case-population control comparisons, in no case did results reach genomewide significance. Of the genes noted as of interest, TMEM108 codes for a transmembrane protein of unknown function, but has previously been reported as associated with smoking cessation in a pooling GWAS study (45). SHANK2 is a scaffolding gene implicated in the formation of the
