In this setting, bortezomib treatment led to inhibition of mammalian target of rapamycin complex 1 (mTORC1, a potent inhibitor of autophagy), increased conversion of LC3-I–LC3-II (a marker of autophagosome formation), and ultimately, autophagy of FLT3 protein.31 Furthermore, autophagy of FLT3 occurred in both quizartinib-sensitive and resistant cells lines, indicating that bortezomib treatment may represent a therapeutic strategy in FLT3-ITD+ AML patients refractory to tyrosine kinase inhibition.31 This evidence concerns the gene FLT3 and acute myeloid leukemia.