This is relevant for CF, where shifting the competitive binding of CBP/p300 in favor of Nrf2 (over NF-kB) leads to increased expression of antioxidant and anti-inflammatory genes and decreased cellular inflammation (Ziady et al., 2012). The molecular mechanisms underpinning the dynamic crosstalk between NF-κB and the Nrf2 are extensively reviewed in (Wardyn et al., 2015) and are still under investigation. The gene discussed is NFKB1; the disease is cystic fibrosis.