Through genetic and pharmacologic validation, we showed that inhibition of XPO1 enhanced the activity of both midostaurin and gilteritinib ex vivo in AML primary patient blasts harboring FLT3-ITD, building upon prior work examining selinexor in combination with the tyrosine kinase inhibitor sorafenib, which has anti-FLT3 activity [11]. Here, FLT3 is linked to acute myeloid leukemia.