This activation, in turn, results in the degradation of the mutated form of tumor protein P53 (TP53), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), an inhibitor of nuclear factor kappa B alpha (IκB-α), and HK2 protein, leading to metabolic catastrophe and cell death in AML cells [57, 58]. This evidence concerns the gene TP53 and acute myeloid leukemia.