Interestingly, in the Apc-shRNA model, the expression of Gli1, Gli2, and Hhip is consistently reduced further in tumours carrying an additional mutation in Kras (Supplementary Fig. 2c), which show higher levels of dysplasia than tumours in Apc-shRNA animals, as well as invasive behaviour, supporting a model in which disrupted tissue architecture interferes with ligand availability and induction of the stromal Hh response21. This evidence concerns the gene KRAS and neoplasm.