In this regard, previous studies reported that the general level of inflammation is increased via constitutive activation of the NF-κB pathway in CF due to CFTR dysfunction that drives higher production of pro-inflammatory cytokines (e.g. IL-8) even in the absence of pathognomonic infectious agents (Vij et al., 2009; Hunter et al., 2010; Wang et al., 2016). This evidence concerns the gene NFKB1 and cystic fibrosis.