Indeed, in zebrafish and murine NB transgenic models, ALK-F1174L expression driven by Dbh or Th promoter, as well as activated ALK KI mutants, did not allowed to confer a fully transformed phenotype to NC derived cells, and thus to induce tumor formation, while co-expression of MYCN was required for NB development [24, 25, 26]. This evidence concerns the gene ALK and neuroblastoma.