Helicobacter pylori infection, a major risk factor for gastric cancer, drives the initiation and progression of mucosal atrophy, intestinal metaplasia, and dysplasia toward gastric cancer via intracellular signaling pathways, such as the interleukin-6- (IL-6-) IL-11-JAK/STAT pathway [1–3]. The gene discussed is IL11; the disease is gastric cancer.