MTOR and acute myeloid leukemia: Some AML clones are dependent on aberrant activation of the mTOR pathway for survival and hence sensitive to clinical mTOR inhibitors, but other clones are resistant [12], and in this study we characterise a cell line (TF-1a) which remained viable in the presence of rapamycin and in which we were able to exploit the dormancy-inducing physiological role of mTOR inhibition [13].