Because primary and secondary glioblastomas have different genetic alterations, notably EGFR and MDM2 amplifications together with p16 deletion in primary glioblastomas and p53 mutation, IDH1 mutation and PDGFR amplification in secondary glioblastomas, the distinct genetic makeup in these two subtypes of glioblastomas could make secondary glioblastomas more susceptible to NovoTTF-100A treatment 20,21. Here, TP53 is linked to glioblastoma.