AKT1 and myeloid leukemia: The proliferation, resistance to apoptosis, and transformation of leukemic cells is mainly due to activation of the PI3K/Akt and NF-κB signaling pathways via oncogenic Bcr-Abl tyrosine kinase in Bcr-Abl(+) myeloid leukemia cells, and this Bcr-Abl expression in the Bcr-Abl(+) myeloid leukemia cell line and K562 cells was inhibited strongly by XH [78].