Common NF-κB-mediated prosurvival mechanisms protect KSHV- and EBV-infected lymphoma cells from apoptosis. In KSHV- and EBV-infected lymphoma cells, apoptosis events are prevented by antiapoptosis, cell signaling, and growth factors regulated by NF-κB (i; NF-κB target genes shown in red). When abrogation of constitutive NF-κB activity occurred (ii), KSHV- and EBV-infected lymphoma cells were sensitized to apoptosis stimuli, and spontaneous apoptosis proceeded through activation of mitochondrial-dependent apoptosis events. Activation of caspases most likely occurred by normal stress stimuli but was enhanced by DNA damage induced in the cells as a result of growth factor deprivation.