We have discovered a regulatory role of miR-200a in controlling formation of sympathoadrenal neurons that involves two very different activities of this miRNA that depend on context. In the neural tube it enforces the epithelial phenotype, maintaining cell junctions and preventing migration. It must be turned off to allow EMT, delamination and migration of neural crest cells. It is turned back on when these cells reach their intended destination, but in that context it drives neuronal differentiation, not reversion to epithelial phenotype. The targets of miR-200 in the epithelial context are well known, but the key target responsible for promoting the neuronal differentiation is not expressed in that context. Since neuroblastoma arises from a failure of neuroblast differentiation, and the miR-200 gene is commonly lost in neuroblastoma, there is a likely role for miR-200 and its target in the disease, and we have supporting evidence for this in mouse orthotopic xenograft experiments using dox-inducible miR-200a. We also have correlative evidence of miR-200a-driven differentiation in neuroblastoma cell lines and its prevention by ectopic expression of a crucial  target in this context.