Dr. Harrison reminds the reader that the polymorphisms used to investigate genetic variation in our study (and others) are of unknown function. Indeed, the T102C marker is a silent T→C base substitution (5), and the variants at the A-1438G locus present similar basal promoter activity (6). Therefore, it is possible that our positive results with the 5HTR2A polymorphisms investigated may in fact be a consequence of underlying linkage disequilibrium between these markers and a functional genetic variant located in a different coding or regulatory region of the 5HTR2A gene. Furthermore, because of the extent of the linkage disequilibrium observed in French Canadians, this functional variant could be located relatively far from the tested polymorphisms (regulatory sequences and enhancers). If this is the case, the other studies may have failed to detect such an effect because, although testing larger samples, they investigated patients selected from nonisolated, panmictic populations, in which the power to detect associations due to linkage disequilibrium is considerably reduced. Certainly, other explanations may be also proposed for the reported inconsistency. Among these are type I error and the different analytical procedures employed. To better understand these issues, we are in the process of collecting a larger and independent sample of French Canadian suicide cases and will attempt to replicate our previous findings.