Together, we propose that a direct binding of components of the T4SS such as CagL (and probably also CagA, CagI, and CagY) to integrin-β1 is to trigger intracellular signaling for bacterial advantage, but also enhance cell attachment and FA formation, thereby supporting the above discussed intracellular activities of CagAPY towards FAK, with the overall goal to prevent excessive cell lifting during the course of infection. This evidence concerns the gene S100A8 and infection.