The functional interplay between BCR/ABL and ABL/BCR may promote the disease in the absence of BCR/ABL inhibition, whereas the functional independence of ABL/BCR as a self-standing leukemogenic factor may contribute to the maintenance of the disease upon an efficient BCR/ABL inhibition and thus to the only transient response of Ph+ ALL patients to the TKI treatment. This evidence concerns the gene ABL1 and acute lymphoblastic leukemia.