CDKN2A silencing is essential for the molecular progression of these TSAs; in spite of the presence of BRAF mutations, these TSAs display a microsatellite-stable phenotype and they originate very aggressive colon carcinomas; (ii) KRAS mutant TSAs are not associated with a precursor polyp and usually are not of the high CpG island methylator phenotype. Here, KRAS is linked to colon carcinoma.