With the loss of anti-inflammatory control, mice deficient in IL-10 overproduce Th1 cytokines,49 develop spontaneous colitis,50 and are prone to produce intestinal tumors in the ApcMin genetic background.51 In ApcMin/+; Il10−/− mice, K. pneumoniae 51–5 increased colonic tumors with significant infiltration of CD3+ cells in lamina propria.20 Involvement of T cell responses, which was derepressed by the deletion of IL-10, was suggested in the K. pneumoniae 51-5-promoted colon tumorigenesis. The gene discussed is IL10; the disease is intestinal neoplasm.