BCR and acute lymphoblastic leukemia: The capacity of ABL/BCR to autonomously induce leukemia suggests that the presence of p40ABL/BCR or p96ABL/BCR contributes to the maintenance of a leukemic subpopulation upon inhibition of BCR/ABL by ATP-analogues such as Imatinib, Dasatinib or Nilotinib, a scenario of particular importance in Ph+ ALL.