In keeping with our previous studies [16]–[18], CXCL8 was chosen as it is generated upon activation of NF-κB and mitogen-activated protein kinase (MAPK)-dependent proinflammatory signaling, and as the principal mediator responsible for neutrophil recruitment is highly relevant to the pathology of asthma and COPD. Here, NFKB1 is linked to chronic obstructive pulmonary disease.