The increase in mTOR that is evident in aggressive tumours, including GBM/GSC, regulates mitochondrial metabolism and cell proliferation via YY1 and YY1-induced peroxisome proliferator-activated receptor γ, coactivator 1α (PGC-1α)[71], thereby contributing to heightened levels of glucose uptake and utilization[72]. This evidence concerns the gene YY1 and neoplasm.