It is known that hyper-activation of the Akt/mTOR pathway sustains the extremely invasive phenotype of GSCs, while mTOR inhibition down-regulates both mRNA, protein levels, and the activity of the matrix metalloproteinases (MMPs) MMP-9 and MMP-2, which promote tumor invasion through extracellular matrix degradation [69]. The gene discussed is AKT1; the disease is neoplasm.