We think there are three possibilities to explain why apoptosisregulating, transcriptional targets of NF-kB, such as death ligands (e.g., FasL and TRAIL) [63, 64] , death receptors (e.g., Fas and DR) [65, 66] , and death-signaling regulators (e.g., Bax and Bcl-X s ,) [67] , were not identified in these studies. First, changes in the expression of prodeath genes activated by reovirus infection may be too transient to have been detected in the intervals selected for analysis. Second, the transformed nature of the cell lines used in these studies may not have been amenable to detection of alterations in gene expression induced by reovirus infection. Third, NF-kB activation following reovirus infection may regulate death signaling at a post-transcriptional level by an as yet unknown mechanism. In support of this idea, levels of DR5 protein increase following reovirus infection [17] but not its mRNA [59] . Additional studies using primary, non-transformed cell lines and genetically engineered viruses that differ only in the capacity to activate NF-kB are required to define how reovirus activates extrinsic apoptotic pathways to evoke cell death.