The Type IV pilus adhesin, CagL, of Helicobacter pylori has recently been shown to induce gastrin production in gastric epithelial cells by adhesion to β5-integrin/integrin linked kinase complexes and downstream signaling through the epidermal growth factor receptor (EGFR), Rapidly Accelerated Fibrosarcoma (Raf) kinase, mitogen activated protein kinase kinase (MEK), extracellular signal regulated kinase (ERK) pathway, thus increasing the acidity of the stomach which can lead to gastric ulcer formation and gastric adenocarcinoma [31]. This evidence concerns the gene EGFR and gastric ulcer.