Although LEN treatment alone did not alter phosphorylating status of BCR-ABL, STAT5, Akt, and Erk1/2, LEN treatment significantly enhanced IM-induced dephosphorylation of BCR-ABL and Akt (D), indicating that LEN renders Ph+ALL cells low activation status in synergy with IM, which might be associated with high susceptibility to apoptosis. The gene discussed is BCR; the disease is acute lymphoblastic leukemia.