Further reports have shown that infection of gastric epithelial cells in vitro resulted in a rapid transactivation of EGFR via matrix metalloproteinase (MMP)-dependent signaling [81,82], regulating various responses including the activation of pro-inflammatory transcription factor NF-κB, cell spreading, anti-apoptosis, and suppression of the H,K-ATPase α inhibiting gastric acid secretion [81,82,83,84,85,86,87]. Here, EGFR is linked to infection.