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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 (IB-), and HK2 protein, leading to metabolic catastrophe and cell death in AML cells [57, 58]

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Rho-kinase, a serinethreonine kinase is known to cause endothelial dysfunction by inactivating eNOS and reducing NO generation (Nohria et al., 2006)

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