Figure 1.

The roles of autophagy in the development and targeted therapy response of AML with FLT3 mutations. FLT3-ITD mutations promote autophagy in AML cells via ATF4, which benefits leukemia cell survival and acquired resistance to FLT3 inhibitors. Coupling FLT3-inhibiting agents with autophagy inhibitors enhances the therapeutic effectiveness for FLT3-mutated AML. Proteasome inhibitors and RET suppression (RET inhibits autophagy by activating MTORC1) can stimulate mutated-FLT3 degradation by enhancing autophagy activity, holding promise as a combinatorial treatment for FLT3-mutated AML