Pituitary adenylate cyclase-activating polypeptide (PACAP) is a regulator of stress response across species.1 Within limbic brain circuits, PACAP signaling coordinates normal physiological stress reactions. PACAP and corticotrophin-releasing hormone work together in the bed nucleus of the stria terminalis (BNST) to modulate anxiety-like behavior.1 We have recently shown that PACAP and a single-nucleotide polymorphism (SNP) of its PAC1 receptor (PAC1R) may be critical mediators of response to psychological trauma. We also reported that this PAC1R gene polymorphism is associated with increased dark-enhanced startle (DES) in adult females but not males with posttraumatic stress disorder (PTSD). We believe these sex differences are because of the location of the PAC1R SNP (rs2267735) in an estrogen response element.2 DES is a known marker of anxiety in adults and children,3–5 and has been shown to be BNST dependent, indicating the potential role of PACAP in increasing DES. We recently found that children of abused mothers show elevated DES.6 Using a sample of children of traumatized mothers, we have extended this research by examining effects of the PAC1R polymorphism on the DES response in these previously non-genotyped children. Based on our study with adults, we hypothesized that genotype would interact with sex to increase DES in girls but not boys. However, we found that the same gene polymorphism associated with PTSD risk in adult females is also associated with increased DES in both male and female children.