TP53 and glioblastoma: NF1 somatic mutations are also identified in approximately 15% of sporadic GBM, with homozygous deletion in approximately 3% and loss of NF1 expression through ubiquitination and proteasomal degradation in another 10–15%.1,21 Loss of NF1 and TP53 together is sufficient to induce high-grade glioma formation in mice.22 Moreover, loss of NF1 expression is associated with sensitivity to MEKi monotherapy in a subset of GBM cell lines, though this was not borne out in a clinical trial.23,24