Attempts to identify genes contributing to liability for PTSD are complicated by the necessity of trauma exposure for the disorder’s symptoms to manifest. Most genetic studies have focused on populations who have experienced specific forms of trauma [e.g., child abuse (Binder et al., 2008), combat (Lawford et al., 2006; Voisey et al., 2009)]. The gene with the strongest evidence reported to date of association with PTSD is FKBP5. Several reports have found evidence of gene-environment interactions involving FKBP5 SNPs and history of childhood abuse (Binder et al., 2008; Xie et al., 2010). Other investigations have found that lower expression of this gene, either measured before (van Zuiden et al., 2012) or after (Yehuda et al., 2009; Mehta et al., 2011) trauma exposure, is associated with greater PTSD risk. The results of association studies of PTSD that examined other genes have been more equivocal [e.g., SLC6A4 (Xie et al., 2009; Goenjian et al., 2012), DRD2 (Gelernter et al., 1999; Lawford et al., 2006; Voisey et al., 2009; Bailey et al., 2010)] or, in some cases, consistently negative [e.g., NPY (Lappalainen et al., 2002)].
