FLT3 and acute myeloid leukemia: The results finally identified several target pairings, holding great promise for systematic combinatorial chimeric antigen receptor therapy of AML.12 In addition, Visconte et al. performed comprehensive quantitative proteomic profiling of the pharmacodynamic changes induced by MLN4924 in MV4-11 FLT3 ITD+ acute myeloid leukemia cells.13 This study evaluated the global impact of inhibiting NEDDylation with MLN4924 on the AML proteome and established rationale for its combination with azacytidine to treat the tumor in vivo.