Consistently, the inhibition of NF-κB/Rel-A in MEFs resulted in decreased oxygen consumption and glycolytic reprogramming, with augmented glucose consumption and lactate production, which is reversed by p53 reconstitution in Rel-A−/− cells, suggesting the indispensable role of NF-κB/p53 axis in metabolic adaptation in normal cells and cancer (149). The gene discussed is TP53; the disease is cancer.