Activation of ALK alone, by point mutation, amplification, or overexpression of the ALKAL ligand, does not appear to be sufficient to drive NB, and either the presence of an additional oncoprotein, such as v-myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog (MYCN), or the loss of critical tumor suppressors is thought to be critical for NB to progress [10,12,13,14,15,16,17,18,19,20,21,22]. Here, ALK is linked to neoplasm.