As the vast majority of NUP98-r cases are also FLT3 mutated,2,21,22 we combined Menin and FLT3 inhibition, which caused a strong synergistic suppression of the expansion of patient-derived NUP98::NSD1 FLT3-ITD double-positive AML cells ex vivo. Here, FLT3 is linked to acute myeloid leukemia.