Since our preliminary data revealed that administration of DNA methyltransferase or histone deacetylase inhibitors resulted in enhanced FOXD3 levels in cultured NB cells, we hypothesize that the down-regulation of FOXD3 in NB may be due to aberrant promoter hypermethylation or histone acetylation, which warrants our further investigation. Here, FOXD3 is linked to neuroblastoma.