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Under stressed conditions, ROS function as secondary messengers which modulate the expression of multiple stress-responsive genes through the activation of various transcription factors

[25] In human cells with mutant WRN, NAD+ repletion restored normal mitophagy, improved fat metabolism, decreased mitochondrial oxidative stress, and enhanced mitochondrial quality

NFE2L2 transactivates multiple genes involved in iron and GSH metabolism, as well as ROS detoxification, thereby limiting oxidative damage (97)

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This suggests the significance of the hydrophobic nature of the interface in the FOXO4 FHD and p53 TAD interaction