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There are countless reports—some in this ARCHIVES—about the association between candidate genes (genes encoding products with neurobiological function such as dopamine receptors, tyrosine hydroxylase, and tryptophan hydroxylase) and a host of behavioral traits ranging from normal personality variants to psychopathologic conditions. Although conflicting results and other inconsistencies have spawned wary commentaries,^1-7 the tide of ‘positive' results continues unabated. In what follows, I highlight pivotal issues in the design and interpretation of association studies, with an eye toward potential pitfalls.

First and foremost, the low prior probability of selecting the ‘right' candidate gene renders the odds of detecting a true-positive finding vanishingly small.^1-3 This stems from the fact that, all genes expressed in the human brain are potential candidates for behavioral traits; there are tens of thousands of such genes. Assuming 20,000 potential candidate loci and a trait governed by 5 vulnerability genes,¹ the P values most commonly encountered in association . . . [Full Text of this Article]