Of note, TCGA data have shown a high prevalence of mutations affecting PTEN in GBM.14 Pre-clinical data have shown a strong association between mutations in PTEN and reduced homologous recombination (HR) function,69 giving a strong pre-clinical rationale for synthetic lethality with poly-ADP ribose polymerase (PARP) inhibitors.70,71 This combined with possible synergy between PARP inhibition and 2 of the core components of standard GBM management, temozolomide, and radiation72,73 and has led to the commencement of clinical trials of PARP inhibitors in GBM which are currently recruiting. The gene discussed is PTEN; the disease is glioblastoma.