The findings reported in the present study have important implications for molecular genetic studies of alcohol dependence, but there are limitations that should be noted. First, the present study was designed to detect loci with moderate effects, and a power analysis suggested reasonable power (0.50–0.60) to detect (logarithm of odds score ≥ 1) a locus that accounts for 20% of the phenotypic variation in the sample. Thus, it is likely that additional genetic loci that exhibited only a small effect on alcohol dependence in the UCSF sample were missed, and it may also explain the lack of support in the present study for loci previously linked to alcohol dependence such as chromosome 4q (Ehlers et al., 2004; Prescott et al., 2006; Reich et al., 1998). Second, multiple statistical tests were conducted in the present study given that we evaluated evidence for linkage using each of the 12 alcohol dependence symptoms assessed by the SSAGA. Corrections were not made to the reported LOD scores to account for multiple testing, but we attempted to control for this in two ways. First, we
