Interestingly, Hatakeyama et al. found that host phosphatidylserine is aberrantly externalised from the inner to the outer leaflet of the host plasma membrane at the site of H. pylori attachment, which facilitates the delivery, intracellular localisation and pathophysiological activity of CagA.36 This finding suggests a mechanism for the release of host phospholipids during bacterial infection.36 Here, S100A8 is linked to bacterial infectious disease.