FLT3-ITD mutations, as well as TKD mutations, led to constitutive activation of FLT3 kinase and triggered several downstream signaling pathways, including the Raf/MEK/ERK pathway, JAK/STAT5 pathway, and PI3K/Akt pathway, which promoted the progression of AML [5]. Here, FLT3 is linked to acute myeloid leukemia.