AKT1 and chronic myelogenous leukemia, BCR-ABL1 positive: The abnormal HSCs in CML are able to survive and thrive through various mechanisms such as modulation of downstream signaling pathways (e.g., JAK/STAT, PI3K/AKT/mTOR, Wnt/β-catenin, Hedgehog signalling), induction of autophagy, selective advantage in homing and engraftment in the bone marrow microenvironment (BMM), and alterations in cellular metabolism [8,15,23,24,25,26,27,28,29].