Considering that (1) the high significance of MCM2 gene expression in survival prediction, (2) the overexpression of MCM2 (and of the whole MCM family) is induced by Myc-N, (3) small molecule inhibitors of MCM2 (ciprofloxacin, lovastatin, trichostatin A, widdrol) are available and already FDA-approved for use in the treatment of other diseases, and (4) the key role played by MCM2 overexpression in the transcriptional instability typical of NB cells [26], we chose MCM2 as candidate for a possible target therapy in a mouse model of NB in vivo. This evidence concerns the gene MYC and neuroblastoma.