Interestingly, caveolin-1 can suppress the transcriptional activity of Nrf2 through direct binding [116], and furthermore, ectopic overexpression of caveolin-1 abrogates both Nrf2 and SOD2 expression in breast cancer, suggesting that the commonly observed loss of caveolin-1 in breast cancer is a driving factor for Nrf2-dependent SOD2 regulation [53]. Here, SOD2 is linked to breast carcinoma.