Three mechanisms are involved in CML oncogenesis, based on BCR-ABL1 activity: (a) altered cell adhesion to the bone marrow stroma and extracellular matrix, (b) constitutively active mitogenic signaling with reduced apoptosis of hematopoietic stem cells and progenitor cells, and (c) genetic instability leading to disease progression [4]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.