Activation of the latter one, also known as the mitogen-activated protein kinase (MAPK) pathway, is mostly driven by oncogenic mutations in BRAF and, to a less extent, in NRAS genes; somatic mutations in such two genes are mutually exclusive and able to stimulate cell proliferation and tumor growth, through induction of a constitutive ERK phosphorylation [1–3]. Here, NRAS is linked to neoplasm.