Nuclear factor-κB (NF-κB) and c-Jun NH₂-terminal kinase (JNK) are activated simultaneously under a variety of stress conditions. They also share several common signaling pathways for their activation in response to cytokines or growth factors. Recent studies, however, demonstrated a new form of interplay between these two allies. Inhibition of NF-κB by ikkβ or rela gene deficiency sensitizes stress responses through enhanced or prolonged activation of JNK. Conversely, sustained activation of NF-κB inhibits cytokine-induced JNK activation. The mechanisms of how NF-κB and JNK become rivals for each other are under extensive debate.