Practically, deregulation of the AKT-FOXO3a pathway has a pivotal role in aggressive NB.23 Recent whole-genome sequence analysis of primary NBs revealed that a higher frequency of somatic mutation occurs only in stage 3 and stage 4 of aggressive NBs.37 Considering that the expression level of BMCC1 was very low in high-risk NB,16 such reduced expression of BMCC1 may mediate genomic instability by attenuation of DNA repair and apoptosis through the hyperactivation of AKT followed by the inhibition of FOXO3a. This evidence concerns the gene FOXO3 and neuroblastoma.