Moreover, the infection of H pylori activated P13K/AKT signaling pathways that were ROS mediated.[19] In addition, H pylori virulence factor CagA can inhibit the proliferation of gastric cancer cells and promote the apoptosis of gastric cancer cells, and its mechanism may be related to the activation of the ERK signaling pathway by CagA.[20] Patients with the same histological types of cancer may have different clinical outcomes due to different of immune cell infiltration.[21] In this study, there was a negative association between the expression of IGFBP1 and CD8 + T cell, DC cell. Here, S100A8 is linked to infection.