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Therapeutic targeting of the NRF2 and KEAP1 partnership in chronic diseases

1 In contrast, in cancer, where malignant cells exploit heightened proteostasis resilience to tolerate genomic instability and therapeutic stress, strategically destabilizing resilience may enhance therapeutic vulnerability

It is possible that the high prevalence in women obeys to a uniparental dysomia or, to the high existing consanguinity or to that the chromosome X containing the normal gene is the one that inactivates itself during the genetic imprints 38