In studies involving sera from 103 Japanese-American men who developed gastric cancer and their matched controls from a longitudinal cohort (26), adding cagA seropositivity to H. pylori status essentially doubled the risk for gastric cancer, especially for the most common intestinal type of adenocarcinoma (OR 2.3 [1.0–5.2]). This evidence concerns the gene S100A8 and gastric cancer.