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The redox and metabolism adaptations to the high oxidative stress environment in cancer cells [1] are manifested by the higher levels in the TNBC cells of the anti-oxidant molecules, GSH and NADPH, the latter which is a major source of reducing equivalent

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A few gene targets of the H 2 O 2 reponsive Yap1 transcription factor were also moderately induced, as noticed elsewhere (Wheeler et al , 2003), but their very limited number, several of which are in fact also controlled by Aft1 (see Supplementary Table S3), and lack of perceptible Yap1 oxidative activation (Figure 5B) indicate at best a very minor activation of Yap1

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