Constitutive KRAS mutations, found in about 50% of all CRCs and in advanced adenomas [40,41,42,43,44,45,46], drive persistent activation of the RAF/MEK/ERK mitogen-activated protein kinase (MAPK) cascade and the PI3K/AKT pathway independently of upstream signals, including the epidermal growth factor receptor (EGFR) [47,48]. Here, KRAS is linked to adenoma.