Taking together our results that EPO-mediated survival correlates with EPOR expression upregulation by kinase inhibitors, an increase of EPOR expression in relapsed tumors, and that EPO is produced by NB [42] and neural crest cells [43] in more than 30% NB tumors [40], we propose that EPOR upregulation is a potential marker for NB tumors, which might escape anticancer therapy and result in a relapse. Here, EPOR is linked to neuroblastoma.