Although the underlying mechanism is still unclear, it is known that RARβ is a necessary component of the inhibitory effects of ATRA on the growth of NB cells [42]; furthermore, RA induces cell-cycle arrest in G1 by decreasing the cyclin-dependent kinase (Cdk) activity required for the G1/S transition and the accumulation of the p27Kip1Cdk inhibitor (CKI) [43], [44] that impair growth and activate the differentiation programme. This evidence concerns the gene RARB and neuroblastoma.