Acute myeloid leukemia (AML) is a heterogeneous disease with cure rates of only 
30-40% in patients <60 years old. Cytogenetic and molecular markers have 
improved our understanding of the different prognostic entities in AML. FLT3 
mutations are present in 30-40% of AML cases, conferring a poor prognosis with 
reduced survival. AXL activates FLT3, impacting adversely on outcome. Both FLT3 
and AXL constitute promising molecular targets. ASP2215 (gilteritinib) is a 
novel, dual FLT3/AXL inhibitor with promising early phase trial data 
(NCT02014558). A Phase III randomized multicenter clinical trial, comparing 
ASP2215 to salvage chemotherapy in relapsed/refractory AML with FLT3-mutations 
is now open to recruitment (NCT02421939). Trial design and objectives are 
discussed here.