The off-target mutation mechanisms are represented by the stimulation of FLT3 downstream signaling pathways, such as the JAK/STAT5 or PI3K/AKT/mTOR pathway in mutated FLT3 AML cells, and like these cascades resulted in lessening the cytotoxic efficacy of FLT3 inhibitors (such as Midostaurin, Sorafenib, and Quizartinib) on AML cell lines [22, 23]. Here, FLT3 is linked to acute myeloid leukemia.