We hypothesized that FLT3 receptor phosphorylation and glycosylation, which have been associated with FLT3 inhibitor resistance, may induce RAC1 hyperactivation, which consequently deregulates of actin dynamics and the antiapoptotic BCL-2 family and may confer midostaurin resistance in FLT3-mutant AML. Here, BCL2 is linked to acute myeloid leukemia.