Primary glioma cell cultures as well as U87 and U251 cell lines where a strong activation of AKT/mTOR pathway was observed exhibited increased sensitivity to rapamycin, the archetypic mTOR inhibitor which did not, however, caused a compensatory AKT activation resulting from mTORC1 negative feedback via insulin receptor substrate (IRS1, Figure 1) [30, 45]. The gene discussed is MTOR; the disease is central nervous system cancer.