MYCN is a member of the MYC family of oncogenes, which also includes c-MYC and MYCL. Despite knowing about the existence of MYCN for nearly thirty years, the majority of functional studies involving MYC family members have focused on c-MYC due to the limited expression profile of MYCN in human cancers, and also in part due to the existence of highly conserved functional domains between c-MYC and MYCN [1]. MYCN is normally expressed during embryonal development and orchestrates cell proliferation and differentiation in the developing peripheral neural crest [2]. However, the deregulated expression of MYCN has been shown to contribute to tumorigenesis and neuronal transformation [3]. Thus, MYCN represents a highly desirable therapeutic target. Previous studies have shown that downregulating MYCN expression, via antisense oligonucleotides, resulted in lower tumour incidence and decreased tumour mass in a murine neuroblastoma tumour model [4]. However, to date, no molecularly targeted therapies have been developed that are able to mimic this response in the clinic, and further studies are required to help elucidate the mechanisms that drive MYCN tumour formation and progression.