The constitutively-activated fusion tyrosine kinase BCR/ABL is encoded by the fusion gene generated by a reciprocal t(9;22) (q34;q11.2) chromosomal translocation causing the Philadelphia chromosome (Ph), which is the molecular signature of chronic myeloid leukemia (CML) and is also observed in 30–40% of acute lymphoblastic leukemia (ALL) [1], [2]. Here, BCR is linked to acute lymphoblastic leukemia.