The present report is part of a larger effort to develop greater consilience between phenotypes for alcohol dependence used in human studies and those used in animal models. The aim of the current set of analyses was to identify a limited set of alcohol-related phenotypes in humans and in mouse by which to compare QTL data between the species using syntenic mapping. The intent of this effort was not meant to be exhaustive but rather to demonstrate how the technique might be applied to a few phenotypes and their QTLs and to identify specific phenotypes in both mice and humans where future studies might improve both data collection and analyses in order to optimize the eventual success of this endeavor. This will contribute significantly to progress in understanding the genetic determination of alcohol behaviors, but there are some limitations. First, the chromosomal regions showing linkage in human and animals studies are often broad and imprecise (at least initially) in terms of their localization of the underlying susceptibility variant(s). Simulation studies have demonstrated considerable variation in the linkage peaks observed for
