Activation of BCR-ABL deregulates cellular proliferation, apoptosis, and genomic stability of primitive CML cells through effects on multiple intracellular signaling pathways such as the JAK2-STAT, RAS and phosphatidylinositol 3-kinase (PI3K) pathways [5, 6]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.