Model of the regulation of DC longevity and death by the balance of JNK/AP-1 and NF-κB activation. DCs enjoy a prolonged lifespan when JNK/AP-1 and NF-κB are activated in a balanced fashion by the ligation of TNFR-SF members. A main function of NF-κB in DCs is to restrict the amount of JNK activity. When NF-κB activation is impaired, TNFR-SF member-induced JNK activity is augmented, and DCs undergo JNK/AP-1–mediated apoptosis. If JNK/AP-1 and NF-κB activities are attenuated simultaneously, TNFR-SF member–induced survival is reestablished. Thus, a balance of JNK/AP-1 and NF-κB activity, rather than the absolute degree of activity amplification of a single pathway, mediates DC survival. Noteworthy is that this model does not rule out the possible absolute requirement of a critical NF-κB signaling threshold for DC survival.