This result contrasts with mechanisms of resistance to other kinase inhibitors (in chronic myeloid leukemia, gastrointestinal stromal tumors, and EGFR-dependent lung cancer), which often occurs through point mutations in the kinase target in tumor cells [43] and raises the possibility that a larger fraction of PTEN null glioblastomas could be rapamycin-sensitive if more significant mTOR inhibition could be achieved. The gene discussed is EGFR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.