KEAP1 and cystic fibrosis: The data on statistically significantly increased and decreased pathways showed the involvement of inflammation-related pathways (Chemokine signaling pathway, Cytokines and inflammatory response, TGFβ signaling pathway), proteases-activated pathways (Osteoclast, Complement and coagulation cascade, Blood clotting cascade, matrix metalloproteinases) and oxidative stress-associated pathways (Oxidative stress, Keap-1-Nrf2, Oxidation by cytochrome P450) (Fig. 3c), which are also known to be associated in CF and COPD pathogenesis1, 2, 3, 4.