Finally, our data suggest that TAK1 may indeed play a critical central role in the activation of IL-8, because infection of gastric epithelial cells with all our H. pylori CagA mutants, in the presence of a TAK1 specific inhibitor [50]-[54], totally abrogated IL-8 secretion, even in the case of the P12CagAKO. The gene discussed is CXCL8; the disease is infection.