For instance, patients with AML harboring FLT3-LTD mutation exhibited pronounced activation of AKT and subsequent phosphorylation of FOXO3a, which inhibited the expression of p27 and the pro-apoptotic protein Bcl-2 interacting mediator of cell death (BIM), facilitating cell cycle progression (Brandts et al., 2005). This evidence concerns the gene FLT3 and acute myeloid leukemia.