As a part of the multi-level validation, we then simulated the impact of common glioblastoma mutations [33] on the distribution of the stable states, including inactivation of PTEN, P27/P21, P53, CDKN2A, and RB, as well as over-expression of Akt, Ras, CDK4, and HIF. The gene discussed is AKT1; the disease is glioblastoma.