We show that patient-derived glioblastoma cells are capable of autocrine/paracrine TNFα-TNFR1 dependent cell death, hence identifying TNFR1, TNFα and NFκB as key targets in this pathway, future work could use drug libraries in order to uncover novel TNFα-sensitising or cytotoxic agents for use in glioblastoma. Here, NFKB1 is linked to glioblastoma.