Notably, whereas oncogenic KRAS activation on its own is unable to initiate intestinal tumorigenesis if not with very late onset and only upon somatic hits at the Tp53 gene [13], compound Apc1638N/+/KRASV12G mice are characterized by a 10-fold increase in tumour multiplicity and by accelerated tumour progression when compared with Apc1638N/+ littermates, with the vast majority of the tumour lesion being represented by adenocarcinomas [14]. This evidence concerns the gene KRAS and neoplasm.