In addition to KMT2A-r, NUP98-r, and NPM1c AML, several other AML subtypes, such as PICALM::MLLT10 or DEK::NUP214 fusions, are characterized by enforced HOXA and/or MEIS1 upregulation and thus potentially sensitive to menin inhibitors [83, 84]. This evidence concerns the gene DEK and acute myeloid leukemia.