A second open question is whether commonly employed NSAIDs (e.g., aspirin, sulindac derivatives; Chan and Detering, 2013; Gurpinar et al., 2014) and NFκB-targeting drugs (e.g., bortezomib, metformin; Hirsch et al., 2013; Zhou et al., 2015) can reestablish stress response-inflammatory thresholds compatible with reparative reprogramming while eliminating aging- and cancer-promoting inflammatory feedback loops. The gene discussed is NFKB1; the disease is cancer.