Recently, clinically relevant improvement of AML therapy could only be achieved either for distinct molecular or cytogenetic subgroups (e.g., midostaurin in FLT3 mutated AML or gemtuzumab ozogamicin for AML with favorable prognosis) or for patients with relapsed/ refractory AML harboring activating FLT3 mutations (e.g., gilteritinib) to replace intensive salvage chemotherapy (Castaigne et al. 2012; Stone et al. 2017; Perl et al. 2019). This evidence concerns the gene FLT3 and acute myeloid leukemia.