Prior serrated tumorigenesis models using conditional activation of a mutant Kras allele in the mouse intestinal tract together with concurrent p16Ink4a/Arf or Pten TSG inactivation(Bennecke et al., 2010; Davies et al., 2014), can promote outgrowth of dysplastic lesions and occasionally progression of some lesions to carcinoma. This evidence concerns the gene KRAS and carcinoma.