Gain-of-function mutations of KRAS, NRAS, BRAF, PIK3CA genes, or loss of tumor suppressor function of PTEN, resulting in continuous activation of RAS-mitogen-activated protein kinase (MAPK) or phosphoinositide 3-kinase (PI3K) pathways, characterize most colorectal cancers (CRC) [1]. This evidence concerns the gene NRAS and colorectal carcinoma.