Rudat et al. showed that mechanistic target of rapamycin complex 1 (mTORC1)-mediated autophagy suppression stabilizes mutant Fms Related Receptor Tyrosine Kinase 3 (FLT3) in AML, while receptor tyrosine kinase inhibition increases autophagy and leads to FLT3 depletion [59]. This evidence concerns the gene FLT3 and acute myeloid leukemia.