The discovery of the BCR-ABL1 fusion oncogene and defining the pathogenetic molecular mechanisms in chronic myelogenous leukemia (CML) have led to the development of BCR-ABL tyrosine kinase inhibitors such as imatinib, nilotinib, and dasatinib, which have improved the 10-year survival rate drastically in CML patients, from 20% to 85% [1–5]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.