BCR-ABL1 oncoprotein stimulates CML LSC self-renewal by increasing the expression of protein phosphatase 2A (PP2A) inhibitors, such as protein SET (SET), cancerous inhibitor of PP2A (CIP2A), and PP2A-Aα, resulting in inactivation of PP2A and MYC overexpression, LSC survival, and the establishment of a positive feedback loop for CML development to BP [57]. The gene discussed is PTPA; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.