Intermittent activation of the alternative NF‑κB kinase NIK restores mitochondrial fitness in exhausted T cells by driving a short‑lived wave of BNIP3‑dependent mitophagy, but only when the signal is followed by a recovery period that allows AMPK‑mediated re‑phosphorylation of ULK1. Continuous IKKβ signaling, in contrast, sustains mTORC1 activity that blocks autophagosome formation and locks cells into a senescent‑like state marked by high PD‑1, TIM‑3 and ROS production. Because PD‑1/CTLA‑4 signaling acts downstream of NF‑κB through SHP2 recruitment (3), removing the chronic IKKβ‑driven inflammatory checkpoint before phosphatase‑mediated inhibition takes place creates a window where a NIK pulse can reset metabolism without being overridden by inhibitory receptors. The hypothesis predicts that (i) inducible, short‑term NIK expression in tumor‑infiltrating CD8⁺ T cells will increase oxygen consumption rate and spare respiratory capacity, reduce mitochondrial ROS, and lower exhaustion markers only if the expression window is ≤6 h followed by at least 12 h of NIK‑off; (ii) prolonged NIK expression (>24 h) will fail to improve metabolism and will instead increase expression of SASP factors such as IL‑6 and IL‑1β; (iii) combining a NIK pulse with a senolytic that clears IKKβ‑high stromal cells will synergistically enhance T‑cell proliferative response to antigen rechallenge compared with either treatment alone. These outcomes can be tested in murine models of chronic LCMV infection or in human tumor‑derived T cells transduced with a doxycycline‑inducible NIK construct, measuring Seahorse mito‑stress, flow‑cytometry for PD‑1/TIM‑3, mitochondrial mass (MitoTracker Green) and membrane potential (TMRM), and cytokine secretion. It's plausible that transient NIK activation mimics the physiological bursts of NF‑κB seen during acute infection, thereby coupling stress signaling to mitochondrial renewal without tipping into chronic activation. A negative result—no metabolic improvement after a brief NIK pulse despite AMPK activation—would falsify the claim that intermittent NF‑κB signaling acts through a mitophagy‑dependent reset, supporting the view that hormetic stressors merely mimic a death‑like state without conferring genuine regenerative capacity. If validated, this approach would suggest that timing‑controlled NF‑κB modulation, rather than continuous hormetic exposure, could be harnessed to rejuvenate T‑cell function in cancer immunotherapy without triggering the deleterious effects of chronic inflammation.