The mouse model that we have developed in this study demonstrates that epithelial TGFβ signalling is tolerated and promotes intestinal tumourigenesis in concert with mutations in Apc and Kras. We next examined whether our model recapitulates the TGFβ-high CMS4 and CRIS-B subtypes of human CRC and, more importantly, whether it resembles the born to be bad, early disseminating lesions characterised by high TGFβ signalling. This evidence concerns the gene KRAS and colorectal carcinoma.