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The interaction of KEAP1 with NRF2 is further modulated by phosphorylation of NRF2 at serine 40 by protein kinase C (PKC).14 Within the nucleus, NRF2 forms heterodimers with v-maf musculoaponeurotic fibrosarcoma oncogene homolog (MAF) proteins (MAF-F, G and K) and binds to antioxidant response elements (AREs) in the promoters of target genes such as those required for glutathione synthesis and its own promoter.15 This activity is regulated by the transcriptional repressor BTB and CNC homology 1 transcription factor (BACH1) which competes for the MAF binding partners and for binding to gene promoters.16 In addition, genetic models suggest that binding of Nrf-2 and its activity are regulated by the ATM substrate, Brca1.17 The most compelling evidence for the role of ATM in redox homeostasis comes from studies of the human radiosensitivity syndrome, Ataxia Telangiectasia (A-T), where both ATM alleles are inactivated

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