The FLT3-ITD mutation causes constitutive activation of the tyrosine kinase domain, resulting in the autophosphorylation of the receptors and consequently in the phosphorylation of substrate proteins which in turn activate downstream pro-survival signaling pathways such as phosphatidylinositol 3‐kinase (PI3K)/protein kinase B (AKT), Ras/extracellular signal-regulated kinase (ERK) and Janus kinase (JAK)/signal transducer and activator of transcription (STAT), promoting the progression of leukemia [4–6]. Here, FLT3 is linked to leukemia.