In agreement with the JAK2 role in mediating Bcr-Abl induction of c-Myc, JAK2 kinase inhibitors, such as AG490, strongly reduce c-Myc expression in CML and induce apoptosis [14, 16], thus indicating JAK2 pathway as an important therapeutic target to overcome Imatinib resistance in CML, a crucial issue in clinical practice [17–19]. The gene discussed is JAK2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.