In addition, Rudat et al. determined, in a large RNAi screen for “rearranged during transfection” receptor tyrosine kinase (RET) effectors, that mTORC1-mediated suppression of autophagy can stabilize mutant FLT3 in AML, while an increase in autophagy was achieved through RET inhibition and led to FLT3 depletion [53]. Here, RET is linked to acute myeloid leukemia.