The reported increase in NFκB induction and activation may be due to the presence of high levels of cytokines which prolong the lifespan of the neutrophil (eg. GM-CSF), the ability of IL-8 and IL-6 (both of which were significantly increased in COPD subjects) to suppress spontaneous apoptosis [46,47] or possibly due to viral and/or bacterial infection. This evidence concerns the gene NFKB1 and bacterial infectious disease.