The results showed modest NF-κB activation upon infection with wild type EPEC, or EPEC lacking active TTSS (ΔescV), whereas the ΔnleBCDE mutant or a mutant deleted of the pathogenicity islands containing these genes (i.e. PP4 and IE6) triggered significantly increased NF-κB activation (p<0.01) (Fig 1A). The gene discussed is NFKB1; the disease is infection.