Notably, among KMT2A fusion partners, MLLT3 and MLLT10 were found in both monocytic AML and AMKL; however, these fusions preferentially show AMKL phenotypes in infants (Fig.S4A), suggesting that AMKL phenotypes are defined both by types of driver alterations and by the developmental stages as discussed in GATA1-driven AMKL in Down syndrome patients59 or GLIS2::CBFA2T3-driven AMKL60. This evidence concerns the gene KMT2A and acute myeloid leukemia.