NFKB1 and gastric cancer: In accordance with this, H. pylori flagellin by influencing the inflammatory milieu trough TLR5 might have a role in gastric cancerogenesis, a hypothesis supported by the demonstration that inflammasome-derived exosomes from GC cells were able to directly activate NF-kB signaling pathway promoting GC [31] and as a consequence of the inflammation, the disruption of the epithelial polarity and integrity of the gastric cells should favor the insertion of H. pylori into the gastric epithelial cells [32], a phenomenon also associated with GC development.