A critical function of AURKA in neuroblastoma is to regulate MYCN protein stability by sequestering MYCN from ubiquitin-mediated proteolytic degradation mediated by the FBXW7 ubiquitin ligase [21], leading us to hypothesize that a down-stream effect of ectopic over-expression PTPRD in neuroblastoma cells would be the destabilization of MYCN. Here, AURKA is linked to neuroblastoma.