While others have shown that araC can enhance mTORC1 activity in AML lines in vitro through hyperactivation of mutant FLT3 in an autocrine or paracrine manner [81, 82], it is possible that in our setting, the lack of mTORC1 activation might relate to the use of the lower concentrations of araC. This evidence concerns the gene FLT3 and acute myeloid leukemia.