After infection with CagA-positive H. pylori, the upregulation of IL-6 and IL-11 expression in GECs depends on non-phosphorylated CagA, and induces STAT3 tyrosine phosphorylation through the gp130 subunit of the IL-6 receptor to manipulate host immunity and promote immune evasion (Jackson et al., 2007; Rizzuti et al., 2015; Hatakeyama, 2017). The gene discussed is S100A8; the disease is infection.