The best known bacterial etiologic agent of gastric adenocarcinoma and colon cancer is represented by Helicobacter pylori. This pathogen promotes tumor onset and progression through multiple mechanisms, including TLR2 upregulation on intestinal epithelial cells and fibroblasts, with the subsequent TLR2-mediated stimulation of their proliferation and EMT through the activation of NF-κB and MAPKs, leading to the secretion of IL-6 [58,107]. Here, NFKB1 is linked to neoplasm.