Interestingly, the tumor suppressor gene phosphatase and tensin homologue deleted on chromosome-10 (PTEN), which is often deleted or inactivated in many solid tumor types [18], [19], [20], has also been shown to be down-regulated by BCR-ABL in CML stem cells, and its deletion can accelerate CML development through the regulation of its downstream target, Akt1 [21]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.