To further understand the overall role of TGFβ signaling in colon cancer development and tumor associated inflammation in vivo, we crossed APCΔ468 (APC) mice (Figure 2a), a model of intestinal neoplastic disease, to those expressing a metallothionein-driven dominant-negative TGFBR2 (MT-TGFBR2DN or TE) to provide a tumor model with strictly epithelial [16] suppression of TGFβ signaling (ATE) (Figure 2b). This evidence concerns the gene TGFBR2 and malignant colon neoplasm.