CML progression is driven by multiple genetic and epigenetic events, including amplification of BCR-ABL1, increased activity of BCR promoter, impaired activity of PP2A, inhibition of SRC homology region 2 domain-containing phosphatase-1 (SHP1) and hyper-methylation of tumor suppressor genes involved in the control of proliferation and survival [31]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.