We therefore opted to begin our investigation using a well‐characterised and isogenic model of cancer development previously shown to be relevant for glioma 33, in which fibroblastic cells are de novo transformed by inactivation of p53 and pRB tumour suppressors and activation of RAS signalling 34, events which recurrently occur in GBM 35, 36(Fig 1A). The gene discussed is TP53; the disease is neoplasm.