In GBM, which is marked by hyperactivation of the PI3K/AKT/mTOR pathway and increased HIF1α induced by oncogenes and hypoxia2, there would be a possibility that the assumed equilibrium of the clock genes and the GBM genes would shift towards the GBM genes, leading to a potentially deregulated clock network and promotion of GBM development. The gene discussed is MTOR; the disease is glioblastoma.