However, the PP2A protein is usually inactivated in CML cells because BCR/ABL stimulates prevention of its auto-dephosphorylation at tyrosine 307 [35, 40] and cancerous inhibitor of PP2A (CIP2A) that has been shown to be overexpressed in CML patients destined to progress to blast crisis mediates inhibition of PP2A [41]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.