A single report suggested that H. pylori-stimulated c-Met phosphorylation in a CagA-dependent manner.[13] To determine if our H. pylori strain stimulated c-Met phosphorylation in a CagA-dependent manner, AGS gastric cancer cells were cocultured for two hours with H. pylori 60190 (Cag PAI+, vacuolating toxin), Tx30a (Cag PAI-, nonvacuolating toxin), or isogenic mutants of H. pylori 60190 lacking functional cagA (60190ΔcagA), cagE (a key functional gene of the TFSS; 60190ΔcagE), or vacA (60190ΔvacA). This evidence concerns the gene S100A8 and gastric cancer.