Our previous work showed that MBZ′s anti-tumor effect in glioblastomas and medulloblastomas is caused by multiple different mechanisms, such as the inhibition of microtubule formation and VEGFR2 autophosphorylation [17,18], which was corroborated by other investigators, applied to various preclinical cancer models and ultimately translated into clinical trials for adult and pediatric patients with cancer (NCT03925662, NCT03628079, NCT02644291, NCT01729260, NCT01837862). This evidence concerns the gene KDR and medulloblastoma.