Mutational activation of Kras alone did not result in skin lesions, nor did deletion of Tgfbr2, whereas the combination of Kras mutation coupled with loss of both alleles of Tgfbr2 resulted in rapid skin tumour formation (LKT mice, Fig. 4d, Median survival 54 days) consistent with our previous observations on deletion of Tgfbr136. This evidence concerns the gene TGFBR2 and skin neoplasm.