Neuroblastoma is one of the most frequent solid paediatric tumours of the nervous system, accounting for up to 10% of all paediatric tumours. The majority of NBs originate from a sympathoadrenal cell lineage of neural crest origin during sympathetic nervous system development, and represent a heterogeneous group of tumours that exhibit a high degree of genetic and biological variability, including not infrequent spontaneous regression or differentiation to ganglioneuroma (Evans, 2004; Nakagawara, 2004). A large percentage of NB patients present with stage 4 disease characterised by dissemination primarily to bone; bone marrow; lymph node; liver and skin sites, with metastatic bone disease carrying automatic stage 4 diagnosis and the poorest prognosis. A subset of stage 4 NBs that disseminate primarily to liver skin and bone marrow sites exhibit frequent spontaneous regression and are classified as stage 4S. Genetic alterations that associated with aggressive NB include: amplification of the proto-oncogenic transcription factor N-myc in up to 20% of all NBs and up to 40% of aggressive NB; gain of chromosome 17 and loss of distal material from the chromosomes 1p32-pter (minimal common region 1p36.2); 14p23-qter; 11q23 and 18, regions likely to contain oncosuppressors (Evans, 2004; Nakagawara, 2004; Jiang et al., 2011; Takita et al., 2000). Despite general improvements in therapy, the age of onset plus high frequency of post-therapeutic relapse have meant that survival rates in patients with NB remain poor, highlighting the need for a greater understanding of the molecular mechanisms involved in this tumor type and the translation of this information into novel therapies. Receptor tyrosine kinases (RTKs) regulate cellular growth, differentiation and survival during development. In general, RTK function depends upon appropriate ligand binding, with inappropriate activation and temporary duration of activation regulated by molecular domain, glycosylation status; protein chaperones; phosphorylation status and associated protein tyrosine phosphatases. The deregulation of RTK function is involved in tumour pathology, with over 30 RTKs associated with different malignancies, and is associated with