We interrogated this core set of defined interactors in the dynamic TH-MYCN transcriptome dataset and showed a strong differential regulation over the course of hyperplastic lesion and full-blown neuroblastoma tumor formation for most interactors (Figure 1F), including the PLK1 kinase, which has a crucial role in MYC protein stabilization [40], and TOP2A that was recently shown to control RNA polymerase II pause release in a dynamic interplay with Aurora kinase A [41]. The gene discussed is MYC; the disease is neoplasm.