To further confirm this, we applied a molecular docking method to evaluate the interaction between the MD average structures of native and mutant FLT3 with type-I and type-II AML inhibitors; Crenolanib, FF-10101, Gilteritinib, KW-2449, PLX3397, Ponatinib, Quizartinib, Sorafenib, Sunitinib, and Tandutinib. This evidence concerns the gene FLT3 and acute myeloid leukemia.