Finally, another potential explanation is that a protein partner of the RelB pathway essential for its full inhibitory activities (e.g. p100/p52 or the aryl hydrocarbon receptor [AhR]) [29] may also be inherently absent or defective in COPD subjects, and thus not allow for the full anti-inflammatory abilities of RelB. The gene discussed is AHR; the disease is chronic obstructive pulmonary disease.