Ras mutants of the canonical ras gene family, H-ras, N-ras and K-ras, are frequently activated by point mutation in human cancers, predominantly at G12, G13 and Q61 residues, leading to impaired GTPase activity resulting in constitutively active mutants persistently binding GTP and promoting tumorigenesis and tumor malignancy [84]. Here, NRAS is linked to cancer.