As the incentive of gastric ulcer, ethanol ingestion in the model mice led to an obvious pathological process compared with that of control mice, which was elucidated by acute gastric mucosal lesions through the neutrophil infiltration, release of proinflammatory cytokines, and the expression of nuclear factor-κB (NF-κB). The gene discussed is NFKB1; the disease is gastric ulcer.