This is of greater importance considering a recent study by Chougule et al. [46], which showed that secondary mutations in FLT3 (ITD and R845G) are responsible for glucocorticoid resistance in ALL and displayed sensitivity to second-generation FLT3 inhibitors both in vitro and in vivo, suggesting that therapies targeting FLT3 might be useful for the treatment of B-ALL-relapsed patients. This evidence concerns the gene FLT3 and acute lymphoblastic leukemia.