focusing only on the promoter region, nor epigenetic mechanisms. Finally, after correction for multiple testing, we also did not reach significance for in-depth investigations of trauma subtypes. We also were not able to totally replicate our results. This issue was possibly related to sample size and reduced power in the replication sample and incomplete comparability between samples. For example, the number of patients with a ‘SS’ genotype in the replication sample was small (n = 29) and had probably reduce our ability to identify an interaction with this particular genotype. Nevertheless, trends for interaction in the larger ‘LS’ genotype group were suggested as shown in the initial sample. Given these limitations, our results will definitively require replication in independent and larger samples of patients with BD. Indeed, the results of gene/environment interaction studies in psychiatry have been a source of controversy, often being hard to replicate or providing mixed results, as in the case of the interaction between 5HTTLPR, stressful life events and the risk of unipolar depression3350515253.
