Conversely, tumor-promoting pathways, such as ERK/mitogen-activated protein kinase (MAPK), NF-κB, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), Ras, STAT3 and Wnt/β-catenin, was activated in CagA-positive H. pylori-infected cells. This evidence concerns the gene S100A8 and neoplasm.