This evidence includes: infection of epithelial cells with a P. gingivalis ΔserB mutant induces less dephosphorylation of NF-κB p65 S536 and higher levels of IL8 promoter activity compared to parental P. gingivalis; ectopically expressed SerB binds to and dephosphorylates p65 in epithelial cells stimulated with TNF-α; exogenous SerB impedes nuclear translocation of p65; and SerB blocks IL8 promoter activity and secretion of IL-8 from epithelial cells. The gene discussed is NFKB1; the disease is infection.