Previous study indicated that knockdown of MYCN induced G0/G1 phase block together with increased expression of P21 in MYCN-overexpressed neuroblastoma cell lines.29 In general, p21 activation is mainly attributed to TP53 activation owing to its binding to the p21 promoter.30 However, in this study, homozygous p53 M133K mutation identified in HEL cells is located in p53 DNA-binding region, and severely impairs the transcriptional regulation of p53 on p21, which indirectly explained the reason for asynchronous expression between TP53 and P21. Here, MYCN is linked to neuroblastoma.