Indeed, several studies have showed that Helicobacter pylori, which is related to more than half of GC cases, is able to penetrate normal, metaplastic and neoplastic epithelia, triggering an immune-inflammatory response, and thus not only promoting gastric carcinogenesis, but also stimulating the release of cytokines, matrix metalloproteinases and angiogenic factors by gastric epithelial cells upon NF-kB activation [13]. Here, NFKB1 is linked to gastric cancer.