Besides, it was found that the expression or activity of pro-apoptotic proteins, e.g., B-cell lymphoma 2 (Bcl-2) antiagonist of cell death (Bad) and Bcl-2-associated X protein (Bax) are inhibited in FLT3-ITD AML cells [56, 57], whereas the expression or activity of pro-survival proteins, e.g., B-cell lymphoma extra large (Bcl-xL), Bcl-2 or myeloid cell leukemia-1 (MCL-1) are upregulated, which is conducive to AML cells’ survival [35, 58–60]. This evidence concerns the gene BAX and acute myeloid leukemia.