Infection with CagA-positive H. pylori strains is the main factor driving the hyperactivity of the PI3K/Akt signaling pathway in gastric cancer, which is due to CagA-induced activation of the PI3K/Akt pathway, the representative downstream MEK/ERK pathway, and the nuclear factor-kappaB (NF-kB) signaling pathway, which subsequently induces the nuclear translocation of beta-catenin [8]. This evidence concerns the gene S100A8 and gastric cancer.