Collectively, our findings provide a rational basis for the combination of the therapeutic antibody dinutuximab with CD47-SIRPα checkpoint blockade to potentiate the antitumor efficacy of neutrophils towards neuroblastomas, at least of adrenergic phenotype, which is expected to significantly improve the dinutuximab responsiveness and patients’ prognosis. The gene discussed is CD47; the disease is neuroblastoma.