One of the mechanisms that can increase the expression of TGF-β in both diseases is oxidative stress; reactive oxygen species that are characteristically found in COPD and rDD pathways [48, 49] may induce TGF-β expression levels, while active TGF-β may induce a redox imbalance and other inflammatory-related molecules through nuclear factor (NF)-κB [50]. This evidence concerns the gene NFKB1 and chronic obstructive pulmonary disease.