The tumor suppressive effect of CASZ1 was initially characterized in neuroblastoma (NB) patients, where a CASZ1 expression anomaly was observed: NB patients are usually accompanied by DNA hypermethylation, histone deacetylation, or 1p loss of heterozygosity that reduces the CASZ1 level, or cytoplasmic mislocalization of the CASZ1 protein that disables its transcriptional role [14,24,26,64]. Here, CASZ1 is linked to neuroblastoma.