Although activation of the mitochondrial UPR [6] may worsen disease outcome, similar to how other stress response mechanisms facilitate tumor progression [20], the profound suppression of NFκB seen under these conditions [6], may open concrete opportunities to re-sensitize resistant tumors to apoptosis-inducing agents, a critical goal of modern cancer therapy [21] (Fig. 2). This evidence concerns the gene NFKB1 and cancer.