CFTR and cystic fibrosis: Moreover, thesame study demonstrated that NF-κB activation (as a marker ofinflammation) and Nrf2 regulation (as a marker of antioxidant response)are effectively corrected by SAHA treatment.16 In agreement with previous studies, SAHA demonstrated the abilityto restore trafficking in misfolded ΔF508 CFTR and to promoteFoxP3+ T-reg activity, thus providing conclusive evidenceof the role of HDAC inhibition in modulation of innate and adaptiveimmune response linked to pathogenesis and progression in CF-relatedinflammatory lung disease.16