To confirm this selective vulnerability on primary human AML in vivo, we transplanted patient-derived xenografts (PDXs) harboring an KMT2A::MLLT3 (MLL-AF9) or KMT2A::AFF1 (MLL-AF4) fusion, into NOD.CgKitW−41JPrkdcscidIl2rgtm1Wjl (NSGW41) animals. This evidence concerns the gene KMT2A and acute myeloid leukemia.