The expression of this enzyme is known to be triggered by CagA-positive H. pylori in infected gastric tissue, promoting the accumulation of various mutations and, in turn, carcinogenesis.60,61 These data also suggest that the reduction of S100-A6, titin, and cytidine deaminase, which are upregulated in gastric cancer and associated with poor prognosis, might be monitored in fecal samples as markers of recovery from H. pylori colonization and resolution of its pathogenetic effects. The gene discussed is S100A6; the disease is gastric cancer.