Given that the increased tumor burden in Mbd4−/− mice (Figure 2D and 2E) did not appear to arise from a greater induction of ACF by AOM, and that DSS induced considerably more severe inflammation-related colitis symptoms in Mbd4−/− mice, we addressed the formal possibility that the greater tumor burden observed in Mbd4−/− mice could be driven by an overactive innate immune response in Mbd4−/− mice. This evidence concerns the gene MBD4 and neoplasm.