Mechanisms which contribute to increased mTOR activity in ALL may be the activation of PI3K/AKT by mutations of the tumor suppressor gene PTEN [17], and by abberant signals from TCL1, BCR-ABL, growth factor receptors (such as IGF-1R and c-kit), IL-7R, flt-3 [18], [19], [20], [21], [22] and oncogenic NOTCH1, the latter one specifically in T-ALL. Here, FLT3 is linked to acute lymphoblastic leukemia.