With respect to the effects of race on our findings, we point out that the analyses of variance (ANOVAs) of the effects of history of childhood abuse and current major depression on hormone profiles throughout the challenges were corrected for the effects of race by introduction of this variable as a covariate. Dunn’s multiple comparison procedures were also adjusted by using pooled mean square errors derived from analyses of covariance. In accordance with the literature (2), we found that race affected ACTH concentrations in the CRF stimulation test. When controlling for the influence of race, we found significant three-way interaction effects of childhood abuse, major depression, and time in all analyses. It is noteworthy that in contrast to our study, previous studies assessing the effects of race on pituitary-adrenal reactivity to challenges did not control for histories of early life stress (2, 3), which may have affected these findings. We considered introducing race as an independent factor in the ANOVAs, resulting in means for different races within the study groups; however, the small number of nonwhite subjects in three of the four groups did not allow for meaningful results. When limiting the group comparisons to white subjects, we were able to support our previous findings (data not shown). We acknowledge that race markedly affects pituitary reactivity and extend Dr. Merskey’s comment by suggesting that race may represent a constitutional factor that interacts with early environmental influences in shaping a phenotype with vulnerability to stress and disease. The role of race in the neurobiology of early-life stress deserves further attention in future studies.