The TFSS was shown recently to interact with the β1 integrin, causing activation of the integrin signaling pathway and facilitating CagA translocation and phosphorylation.[35] We previously showed that activation of the β1 integrin also leads to downstream activation of JNK and paxillin, both of which are required for H. pylori-induced cell motility.[26] These data demonstrate that H. pylori stimulates gastric cancer cell motility through a combination of CagA-dependent and CagA-independent signaling. This evidence concerns the gene S100A8 and gastric cancer.