However, either EPHA3 knockdown or EPHA3 kinase activation through binding to Ephrin A5 or an agonist antibody, resulted in a significant reduction of the growth of glioblastoma cells28, suggesting that in these tumors EPHA3 has ligand/kinase-independent oncogenic activity and ligand/kinase-dependent tumor suppressor activity. The gene discussed is EFNA5; the disease is neoplasm.