In addition, via the use of shRNAs that reduce the expression of key autophagy proteins, it was shown that autophagy is required for the proliferation of AML cells in a murine model, giving autophagy a protumorigenic role and showing that its inhibition exceeds the resistance to the FLT3 inhibitor quizartinib [145]. This evidence concerns the gene FLT3 and acute myeloid leukemia.