Our group was the first to demonstrate that at the protein level the two central components of the alternative pathway, p100/p52 and RelB, were overexpressed in primary NSCLC lesions compared to adjacent non-neoplastic lung parenchyma and normal, cadaveric lung tissues in individuals who have never been exposed to cigarette smoke17. The gene discussed is NFKB2; the disease is non-small cell lung carcinoma.