Pathogenic strains of H. pylori, associated with the development of adenocarcinoma in humans, inject CagA into gastric epithelial cells, where it interacts with many different host cell proteins (e.g. Abl kinases, SRC, PAR1b/MARK2 kinases, CrkII, SHP-2 protein tyrosine phosphatase), interfering with signalling pathways that regulate cell growth and motility [5–10]. The gene discussed is PTPN11; the disease is adenocarcinoma.