Certain limitations should be kept in mind when interpreting findings from the present study. First, although the categorization of low- vs high-risk traumas closely parallels the assaultive vs nonassaultive distinctions used in the larger trauma literature, the finding that combat exposure did not confer high risk for PTSD is inconsistent with studies conducted with US samples. This inconsistency is likely due to differences in military experiences between these US samples and that of the present study (whose age precluded participation in Vietnam and for whom assessment largely preceded recent conflicts [ie, Afghanistan and Iraq]). It does make an important point that research using broad categories of traumatic events must be interpreted with consideration of the distribution of exposure severity represented and, perhaps, the population-specific perception of individual events. It is possible that the sample-specific empirical categorization of trauma risk may have contributed to the magnitude of the overall association observed between high-risk trauma and PTSD. Second, the design included oversampling of families in which twins reported childhood maltreatment. Thus, to the extent that the relationship between trauma and MDD in this high-risk group differs from that in the general population, generalizability of these findings may be limited. However, results of the analyses we conducted with the community-based full cohort II sample suggest that any ascertainment bias likely had a very limited impact. Third, the ordering of variables had some effect on the heritability estimates obtained from the final reduced model. Estimates of heritability robust to the order of the first 3 variables, derived from the saturated AE model (shown in eFigure 1), are 36% for MDD, 46% for low-risk trauma, and 58% for high-risk trauma. Thus, the heritability for MDD calculated from the reduced model may have been slightly reduced. Fourth, given the aim of characterizing heritability and overlapping genetic influences on trauma exposure, MDD, and PTSD, twins make up a large proportion of the sample. Although they compose a small minority of the general population and they differ from singletons with respect to certain health outcomes in childhood, these differences are not significant beyond age 5 years45- 46 and are, therefore, unlikely to influence the outcomes of interest in this study. Fifth, although the DZ twin, sib-twin, and sib-sib correlations are similar, the models include an assumption of their overall equality. A reduction in resemblance for these phenotypes in nontwin siblings, vs that of DZ twin pairs, would reduce the estimate for comparison with MZ twin pairs and, consequently, inflate estimates of genetic effects. Sixth, given that PTSD and MDD have partially overlapping symptoms, diagnostic imprecision could have contributed to the estimates of shared vulnerability that we obtained. Seventh, the approach of coding individuals with no history of trauma exposure as missing for PTSD, consistent with DSM-IV Criterion A, clearly affected the findings. The alternative, coding them as not meeting criteria for the disorder, would have added solely to those cells containing individuals without PTSD and each type of trauma exposure, thus increasing the magnitude of correlations between each trauma type and PTSD and the respective estimates of their total shared variance. The present approach reduced the number of comparisons informative for calculating parameter estimates for PTSD and, thus, limited our ability to examine alternative models (eg, obtaining separate estimates for women and men). Eighth, given the sample's complex family structure and sample size constraints, we used models that controlled for the main effect of sex. By doing so, we may have failed to detect underlying genotype× sex interactions.