The phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) and mammalian target of rapamycin (mTOR) pathways are shown to be constitutively activated in 50–75% of T-ALL.141 Preclinical studies suggest that inhibition of the PI3K/AKT/mTOR pathways may be an effective treatment for T-ALL.142, 143, 144, 145 A dual PI3K/mTOR inhibitor, NVP-BEZ235, potently inhibited the proliferation ALL cells in vitro, causing G0/G1 arrest. Here, MTOR is linked to acute lymphoblastic leukemia.