al., 2008). Interestingly, at the height of our Finnish multipoint peak, around 20 cM, Wang et al. (2005), reported a genomewide significant linkage peak, using a quantity smoked phenotype measured in the Framingham Heart Study. At both 31cM and 74 cM He et al. (2008), recently reported suggestive linkage peaks using measures of cotinine pharmacokinetics. Between our linkage peaks from 40 cM to 100 cM on chromosome 11, at least four studies have reported linkage signals using smoking-related phenotypes (Morley et al., 2006; Li et al., 2003; Li et al., 2006; Bierut et al., 2004): with the highest linkage signals detected in this region using quantity smoked measures in African American, Australian and the US-based Framingham Heart Study families (the later two being predominantly Caucasian ancestry), respectively. Bierut et al. (2004) found a LOD = 1.6 at 87 cM using a habitual smoking phenotype in families targeted for alcohol dependence. Finally, near our peak for the Australian sample on 11q, Gelernter et al. (2007) reported a two-point LOD = 1.97 at 109 cM for DSM-IV nicotine dependence in a U.S. Caucasian sample ascertained for cocaine or heroin dependence.
