As we consistently detected enhanced levels of HE4 in the presence of abnormal CFTR function in CFBE 41o− cells bearing F508del-CFTR in contrast to wt-CFTR cells under non-activated and TNF-α activated conditions, we raised the question whether increased HE4 expression in CF is under the regulation of NF-κB mediated pathway directly via impaired CFTR function and related pro-inflammatory stimuli. The gene discussed is NFKB1; the disease is cystic fibrosis.