Several studies in TERT-mutant glioblastomas demonstrated that GABPA, an ETS factor acting as a tetrameric protein along with its GABPB isoform, drives TERT-mutant transcription in this tumor lineage, opening the door to targeting the GABPA/GABPB axis to achieve TERT downregulation in that context [13,14,15]. The gene discussed is TERT; the disease is glioblastoma.