PLD1 expression and IκBα phosphorylation are aberrantly increased in H. pylori-infected human gastric cancer tissues, and rebamipide, a mucosal-protective antiulcer agent, abolishes H. pylori cagA-induced PLD1 expression via inhibition of NF-κB binding to the PLD1 promoter. The gene discussed is NFKB1; the disease is gastric cancer.