Reduced abundances of protein S100-A6, myosin-2, annexin A11, actin, tubulin alpha-1A chain, and annexin A4 were also consistent with their role in cytoskeletal rearrangements and H. pylori disruption of the barrier function, as previously reported.52–56 Furthermore, among proteins with reduced relative abundance at T1, we found fecal albumin, a good indicator of a disrupted intestinal barrier, and titin, a structural protein related to H. pylori infection and gastric cancer.57–59 Finally, cytidine deaminase activity was significantly reduced at T1. The gene discussed is MYH2; the disease is gastric cancer.