For example, one study demonstrated that epithelial NF-κB activation could promotes the initiation of lung cancer by upregulation of anti-apoptosis gene Bcl-2 expression [52]; In contrary, another study revealed that short-term NF-κB inhibitor, bortezomib might promote lung caicinogenesis, but prolonged NF-κB inhibition could enhance chemical-induced initiation of lung cancer by increased expression of inflammatory cytokine/chemokines, such as interleukin-1β, CXCL1 and CXCL2 [53]. The gene discussed is CXCL1; the disease is lung carcinoma.