Among the generated mouse genotypes, double mutations of ApcΔ716Tgfbr2−/− and ApcΔ716Trp53+/R270H resulted in the development of invasive adenocarcinoma in the intestine, suggesting that Wnt signaling activation in combination with TGF-β suppression or the expression of mutant p53 R270H induces submucosal invasion (Figure 3), while ApcΔ716KrasG12D combination is not sufficient for generating an invasive phenotype. This evidence concerns the gene TP53 and adenocarcinoma.