conducted a within-group comparison of neighborhood controls who were and were not illicit drug dependent. A conservative Bonferroni correction for multiple testing yielded a revised significance threshold of P = 3.9 × 10−6 (i.e., .05 /1430 SNPs/ 9 phenotypic comparisons: [1] cases vs. neighborhood controls; [2] cases vs. ATR controls; cases vs. neighborhood controls not dependent on [3] illicit drugs, [4] illicit drugs or alcohol, and [5] illicit drugs, alcohol, or nicotine; cases vs. neighborhood controls dependent on [6] illicit drugs, [7] illicit drugs or alcohol, and [8] illicit drugs, alcohol, or nicotine; and [9] neighborhood controls dependent on illicit drugs versus neighborhood controls not dependent on illicit drugs). We controlled for the allelic dosage of the most strongly associated SNP to examine whether a single signal adequately explained all observed chromosome 11 gene cluster associations. Consistent with prior reports that focused on haplotypes spanning these genes, we conducted analyses using SAS version 9.2 37 statistical software (SAS Institute, Inc.) to characterize risk (i.e., additive, dominant, or recessive) associated with each of the two SNPs for whom independent signals were found. To estimate their effects in tandem, we coded a risk level variable that was a sum of their effects.
