KRAS and NRAS mutations appear early in colorectal carcinogenesis (aberrant crypt foci lacking dysplasia and polypsis) leading to constitutive signaling and downstream activation of mitogen-activated protein kinase (MAPK) and phosphoinositide 3- kinase (PI3K) dependent pathways [2–4], and contribute also to tumor progression in association with others genetic alterations [5]. This evidence concerns the gene KRAS and neoplasm.