Given that N-Myc is dominant in patients with MYCN-amplified neuroblastoma, whereas its highly homologous protein C-Myc plays a role in patients with non-MYCN-amplified disease (29–31), as also indicated by their specific expression and CRISPR sensitivity (Supplemental Figure 1, B and C), we suspected that KLHL37 might also have a regulatory effect on C-Myc that would explain the poor prognosis of patients with non-MYCN-amplified disease. The gene discussed is MYCN; the disease is neuroblastoma.