Our paper exhibits that ethanol administration-induced gastric ulcers in rats are strongly related to oxidative stress and inflammatory responses; the elevation in the level of oxidized glutathione (GSSG) and the decrease in the activities of key enzymes, involving glutathione peroxidase (GPX) and catalase (CAT); and also, the disruption in gastric secretory functions including suppressed gastrin levels and elevated inflammatory mediators like histamine, TNF-α, and NF-κB. This evidence concerns the gene NFKB1 and gastric ulcer.