This study demonstrates a potential mechanism by which sEVs derived from cisplatin-resistant neuroblastoma cells modulate endothelial cell function through alterations in metabolic pathways and provides an opportunity to explore exosomal MYCN and glycolytic proteins for developing circulating biomarker signatures that could enable more accurate disease diagnosis and monitoring, as well as tailored treatment approaches. The gene discussed is MYCN; the disease is neuroblastoma.