Furthermore, the EPHB4-V871I variant contributed to increased proliferation, migration, and invasion properties in neuroblastoma cell lines via increased phosphorylation of the ERK1-2 pathway and effects on the vascular endothelial growth factor (VEGF), c-RAF, and cyclin-dependent kinase 4 (CDK4) target genes, while treatment with EPHB4 inhibitors reversed the phenotype driven by the variant, suggesting an option for therapeutic targeting in neuroblastoma [106]. Here, EPHB4 is linked to neuroblastoma.