This scenario is consistent with recent findings showing that a loss of caveolin-1 expression in breast cancer cells activates nuclear erythroid 2 p45-related factor-2 (Nrf2) and promotes manganese-dependent superoxide dismutase (MnSOD)-induced glycolysis and that reconstitution of caveolin-1 expression in caveolin-1-negative breast cancer cells suppresses Nrf2, reduces MnSOD expression, inhibits glycolysis and enhances mitochondria-dependent ATP production [41]. The gene discussed is CAV1; the disease is breast cancer.