Intracellular CagA can undergo tyrosine-phosphorylation or remain unphosphorylated; in either form, CagA aberrantly activates numerous signaling pathways which can induce proinflammatory responses.2–4 However, only a subset of persons infected by cag-positive strains ever develop cancer,5 underscoring the importance of defining precise interactions that increase gastric cancer risk. The gene discussed is S100A8; the disease is gastric cancer.