Although our mapping results provided weak evidence for linkage of smoking rate to chromosome 20 (p = 0.0063; see Table 2), this locus appears to be interesting. Using the same Framingham Heart Study data, two other research groups [11,12] independently reported weak linkage of the maximum number of cigarettes smoked per day across the first four exams or across all exams of the original and offspring cohorts onto the same region of chromosome 20 identified in this study. To our knowledge, no previous studies in the literature have identified linkage or association with this region on chromosome 20. Therefore, it will be of interest to confirm this finding in other studies. The reason that we achieved lower p-values for most regions reported in our study than other GAW13 analyses evaluating smoking as the phenotype may due to how the data measuring smoking phenotype were selected from the Framingham Heart Study data. As indicated earlier, we only used the smoking information obtained from the exam conducted during 1970–1971, instead of using the maximum number of cigarettes smoked per day across multiple
