Given the primary effect of NF1 loss is Ras misactivation, we rationalized that conserved genetic perturbations mediating growth or MEK inhibitor response across both NF1-mutant human GBM43 and Nras-mutant mouse SB28 models would reflect robust and reproducible mechanisms underlying NF1-mutant glioblastoma biology. The gene discussed is NF1; the disease is glioblastoma.