This state is facilitated by activated oncogenes including MYCN, which is amplified in approximately 20% of primary NBs and carries poor prognosis [23,24]; the hypoxia-regulated oncogenic alternative TrkAIII splice variant of the neurotrophin receptor tropomyosin-related kinase A (TrkA), which exhibits spontaneous intracellular activation and is expressed in advanced stage, relapsed, and metastatic NBs [25,26], aberrant neurotrophin receptor TrkB expression [27], and oncogenic ALK activation [28], to name a few. This evidence concerns the gene ALK and Nijmegen breakage syndrome.