In addition, infection of HEK293 cells expressing TLR5 with H. pylori induced the phosphorylation of IL-1 receptor-associated kinase 1 (IRAK-1) and inhibitor of kappa B (IκB), and this was required for the activation of NF-κB. However, induced expression of transfected TLR5 in HEK293 cells shifted cagPAI dependent to cagPAI independent proinflammatory signaling for the secretion of IL-8 and TNF-α [34]. The gene discussed is TLR5; the disease is infection.