AKT suppresses mitochondrial apoptosis through phosphorylation-dependent inactivation of proapoptotic factors BAD22 and FOXO3a (forkhead box-O3a),23 a forkhead box-O transcription factor that contributes to apoptosis induced by BIM.24 Moreover, hyperactivation of AKT pathway occurs frequently in cancers,25 and increased AKT phosphorylation correlates with poor prognosis in NB.23, 26 However, extremely little is known about the mechanism with which BMCC1 promotes apoptosis and modulates signaling pathway via the BNIP2 homology region. This evidence concerns the gene PRUNE2 and neuroblastoma.